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topic 6 Flashcards

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1
Q

what factors affect the rate of decomposition

A
  • temp
  • oxygen availability

these speed up enzyme activity
intense heat denatures enzymes involved in autolysis

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2
Q

what happens hours after death

A
  • body temp dec.
  • bacteria + enzymes decompose body cells + tissue→ this is called autolysis
  • fly eggs present
  • rigor mortis (4-6 hours after death)
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3
Q

recall the process of how rigor mortis occurs

A

-muscles deprived of O2
-anaerobic respiration→ causes a build up of lactic acid
-pH in cells dec.
-enzyme activity inhibited
-no ATP produced
-bonds between myosin and actin break
-muscles become fixed

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4
Q

what occurs days after death

A
  • microorganisms decomposes tissue + organs→ self digestion
  • discoloration of skin of lower abdomen- first sign of decomposition (putrefaction)

discoloration will spread across body + darken to reddish green and then purple-black
methane released so body bloats + skin blisters

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5
Q

what happens weeks after death

A
  • tissue liquefied + fluid seeps out
  • body no longer stiff
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6
Q

what is left months and then years after death

A

skeleton- months
skeleton disintegrates- years

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7
Q

what temp and degree or rigor mortis is the body at 3 hours after death

A

warm, not stiff

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8
Q

what temp and degree or rigor mortis is the body at 3-8 hours after death

A

warm and stiff

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9
Q

what temp and degree or rigor mortis is the body at 8-36 hours after death

A

cold and stiff

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10
Q

what temp and degree or rigor mortis is the body more than 36-48h after death

A

cold and not stiff

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11
Q

what is algor and rigor mortis
What does core temp depend on

A

algor mortis- cooling of body after death
cooling of the body follows a sigmoid curve
- core temp depends on ambient temp
- ambient temp fluctuates over time

rigor mortis- stiffening of muscles after death
smaller muscles stiffen first during rigor mortis

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11
Q

what are the factors affecting post-mortem cooling

A
  • body size
  • body position
  • clothing
  • air movement
  • humidity
  • temp of surroundings
  • body temp measured via rectum or abdomen
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12
Q

what is forensic entomology and how can it be used to determine time of death

A

Forensic entomology- presence of insects used to estimate how much time since death
- determine rate of maggot development can be determines using maggot mass, temp of air around body
- determine age of maggots + time eggs were laid gives a minimum time since death

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13
Q

what are the changes in insects present as the body decomposes

A

after death= bacteria
decomposed tissue= flies + larvae
dry tissue= beetles, flies leave
no tissue= no organisms

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14
Q

what is succession in terms of decomposition

A

as one group of organism feeds on a decomposing body, conditions change in a way that is attracts another group of organisms due to bacterial decomposition which makes the body suitable for different insects

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15
Q

how do forensic entomologists use succession of organisms on a corpse to determine time of death

A

forensic entomologists use sequence of organisms feeding on body to determine time of the death by seeing what stage of the life cycle the insects colonising the body are at, which can be used to determine age of maggots and estimate the time the eggs were laid

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16
Q

what is an example of an investigation that can be used to study the effect of temperature on the time taken for the first instar maggot to become a pupa

A

1) use a range of temps
2) water bath
3) timing starts when eggs hatch into instar maggots + ends when the third instar maggots begin to pupate
4) provide food for maggots
5) control humidity

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17
Q

what are the conditions that affect the life cycle of an insect

A
  • dugs
  • humidity
  • oxygen
  • temp
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18
Q

what is the effect on temp on the rate of decomposition

A
  • low temp- slows down decomposition
  • warm temps speed it up
  • highest rate between 21-38C
  • intense heat denatures enzymes involved in autolysis which delays decay
  • injuries→ bacteria can enter body which aids decomposition
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19
Q

what is DNA profiling used for

A

used for the identification + determining genetic relationships between organisms + plants

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20
Q

what is PCR used for

A

DNA can be amplified using the polymerase chain reaction

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21
Q

what are exons

A

sequences that contain the code for a peptide (protein) and are expressed

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22
Q

what are introns

A
  • non coding sequences of mRNA
    a large amount of DNA doesnt code for proteins
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23
Q

recall the process of post transcriptional modification

A
  1. 1 gene codes for more than one protein
  2. this is due to alternative splicing of exons- different combinations of exons form
  3. this happens in the spliceosome
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24
Q

what are STRs

A
  • with introns, you have short tandem repeat sequences (STR) also called satellite DNA
  • an STR can contain from 2-50 base pairs and can be repeated from 5-several hundred times
  • more similar repeats= more related
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25
Q

what do the exons do during transcription

A

During transcription exons join to form mRNA

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26
Q

what is pre mRNA made up of

A

pre-mRNA is mRNA with introns + exons

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27
Q

how do you extract DNA from plant material

A
  1. tissue sample is physically broken down in a buffer that includes salt a detergent to disrupt the cell membranes
  2. the small suspended particles including the DNA are separated from the rest of the cell debris by filtering or centrifuging
  3. protease enzymes are incubated with the suspension to remove proteins and then cold ethanol is added to precipitate out the DNA
  4. stages of washing the DNA in a buffer solution then follow
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28
Q

what is the role of a restriction enzyme in PCR

A

cut dna using restriction enzyme - scans DNA until it finds a specific sequence/site and cuts it into fragments
if enzyme cuts at two points- gives three fragments
dna cut with the same restriction enzyme have the same sticky ends so come back together

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29
Q

what is gel electrophoresis used for

A

used to figure out the size of DNA

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30
Q

what is the process of gel electrophoresis

A

-has wells where you insert DNA
-positive charge at the bottom
-dna is negative and is pulled down by the positive charge as it is attracted
-smaller fragments travel further than larger fragments
-sorted according to length of proteins

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31
Q

what is the role of a primer

A

bonds to complimentary site on DNA, grabs onto dna and allows taq polymerase (can withstand high temps) to drive DNA down and copy the DNA

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32
Q

what is taq DNA polymerase

A

Taq DNA polymerase is a temperature resistant enzyme responsible for dna replication by assembling nucleotides along a complimentary strand
artificial complementary sequences of DNA that latch onto the desired sequences so that DNA polymerase can attach to the strand and begin synthesising a complimentary strand

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33
Q

what is the role of fluorescent markers

A

allows you to see how much DA has been amplified, this is different to the gel electrophoresis markers

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34
Q

what is the role of nucleotides in PCR

A

to synthesise new complimentary strands of DNA

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35
Q

what is recombinant DNA

A

DNA that has been formed artificially by combining DNA fragments from different organisms

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36
Q

recall the sequence of events of PCR

A
  1. a sample is treated with detergent to break open cells + release the DNA
  2. DNA primers- DNA polymerase, DNA primers with fluorescent markers and nucleotides added to reaction tube which is put into the PCR thermal cycler
  3. 95C- the DNA strands separate
  4. 55C- primers attach at the start of each STR sequence
  5. DNA polymerase attach and replication occurs from each primer. in each cycle that follows the process is repeated producing copies that are just the STR sequence fragment. millions of these STR fragments are produced and can be separated out by gel electrophoresis
  6. steps 3-6 are repeated in a cycle
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37
Q

at what temperature does the DNA strands separate in PCR

A

95C

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38
Q

at what temperature do primers attach to the start of each STR

A

55C

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39
Q

how do you work out how many DNA molecules are produced in x amo8unt of cycles

A

you do 2 to the power of however many cycles

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40
Q

what is the difference between taq polymerase and human enzymes

A

taq polymerase can withstand high temperatures and is used to synthesise new DNA strands through complimentary base pairing

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41
Q

what is DNA fingerprinting

A

analyses short tandem repeats/ introns
used for investigating crime scenes
assumes every individuals DNA is unique

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42
Q

how is DNA fingerprinting carried out

A
  • sample of DNA is extracted and purified
  • PCR carried out to amplify the STR
  • different length STRs are separated using gel electrophoresis (similar to chromatography)
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43
Q

how is gel electrophoresis used to determine size of molecules

A
  • separate molecules based on size
  • DNA moves through the gel which provides the medium of fragments to move to the positive electrode
  • shorter STRs travel further than longer STRs since they have a higher molecular weight
  • DNA ladder has known fragment sizes
  • the unknown DNA bands are compared to the known weights on the ladder to estimate their weights
  • the DNA can be dyed to compared to a molecular weight band
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44
Q

how are DNA profiles compared

A
  • compare total number of bands
  • compare position of bands
  • compare sizes of bands
  • number of bands that match the sample indicate similarity of DNA
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45
Q

what are VNTRs

A

repeated sequences + occur in non coding regions

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46
Q

what is the role of southern blotting

A

makes the banding pattern more stable- the DNA is transferred to a nylon membrane to be viewed

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47
Q

why may DNA profiling results may not be absolutely conclusive

A
  • DNA profiling has several stages
  • contaminations can arise at any stage
  • only a small portion of DNA is analysed
  • possibility of two identical profiles from unrelated individuals
  • identical twins may show identical profiles
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48
Q

what are pathogens

A
  • pathogens cause damage by taking nutrition from the host
  • a pathogen is any organism that causes disease
    diseases caused by pathogens → infectious diseases
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49
Q

how do bacteria damage cells

A
  • belong to prokaryote kingdom- no nucleus
  • damage cells by releasing toxins
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50
Q

recall the organelles in bacteria

A

flagella
pili
bacterial chromosome
plasmids
capsule
plasma membrane
cell wall
ribosomes

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51
Q

what is the role of the flagellum

A

rotates to make bacteria move

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52
Q

what is the role of pili

A

help bacteria stick to other cells and can be used in gene transfer

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53
Q

what is the structure of bacterial chromosomes in the cytoplasm

A
  • dna floats free in the cytoplasm
  • most of the dna is in one long coiled up strand
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54
Q

what are plasmids

A

small loops of DNA that arent part of the chromosome

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55
Q

what are plasmids

A

small loops of DNA that arent part of the chromosome

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56
Q

what are mesosomes

A

also may contain folds called mesosomes

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57
Q

what is the role of the cell wall

A

supports the cell

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58
Q

how do viruses attack

A

invade cell and take over the organelles and genetic material

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59
Q

what is the structure of viruses

A

made up of DNA or RNA which is the core nucleic acid
capsid
envelope
attachment protein
protein inside capsid

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60
Q

what does the capsid of a virus do

A

carry proteins inside their capsid

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61
Q

what is the role of attachment proteins on viruses

A

attachment proteins stick out from their capsid and let the virus cling to a suitable host

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62
Q

what is the envelope

A

outer layer which is stolen from the cell membrane of the previous host cell

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63
Q

what is the role of the protein coat

A

capsid which protects the DNA/RNA

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64
Q

what are the characteristics of viruses

A
  • no ribosomes
  • lack of internal structures
  • small
  • strand of either RNA or DNA
  • cant replicate without a host
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65
Q

what is HIV and what does it do

A

HIV- human immunodeficiency virus:
- infects and destroys a type of white blood cell→ destroys T-helper cell
- T helper cell activates other immune system cells

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66
Q

How does HIV destroy T-helper cells and why does it do this

A

they acts as a host for HIV as it replicates inside the cell (can only reproduce this way)
HIV doesnt have organelles to replicate on its own which is why it uses the organelles of the host cell

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67
Q

how does HIV spread

A
  • is spread through infected bodily fluids
  • when these fluids come into contact with mucosal surfaces or damaged tissue or injected into blood stream infection occurs
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68
Q

how does HIV replicate

A
  • attachment protein which is a glycoprotein called gp120 attaches to receptor on cell membrane of T helper cell
  • capsid of HIV released into the cell, uncoats and releases its genetic material into the cells cytoplasm
  • reverse transcriptase makes a complimentary strand of DNA from the viral RNA template
  • from this double stranded DNA is made and inserted into human DNA
  • host cell enzymes are used to make viral proteins from the viral DNA found within the DNA
  • viral proteins are assembled into new viruses which burst from the cell and go onto infect other cells
    it replicates rapidly
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69
Q

what is the latency period

A
  • latency period- HIV replication drops to a lower level after the period of rapid replication
  • during this period the infected person wont experience any symptoms
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70
Q

what does HIV cause

A

HIV causes AIDS
AIDS- acquired immune deficiency syndrome

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71
Q

what is AIDS

A

this is when the immune system deteriorates and eventually fails
when symptoms of a persons failing immune system start to appear or their T helper count drops below a certain level they are classified as having AIDS

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72
Q

what is opportunistic infection

A

opportunistic infection- when people with AIDS develop diseases and infections that wouldnt usually cause serious problems in people with a healthy immune system

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73
Q

What are the initial symptoms of aids and how does AIDS progress

A
  • initial symptoms of AIDS- minor infections of mucous membranes which is caused by low T helper cell count
  • as AIDS progresses, number of T helper cells decreases further. patients become more susceptible to serious infections such as tuberculosis
  • late stage of AIDS- very low number of T helper cells and suffer from a range of serious infections which kill the AIDS patients rather than HIV itself
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74
Q

what factors affect the progression and survival of AIDS

A
  • existing infection
  • the strain of HIV they’ve infected
  • age
  • access to healthcare
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75
Q

which bacteria causes tuberculosis

A

mycobacterium tuberculosis

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76
Q

how is tuberculosis contracted/spread

A

when tiny droplets containing the bacteria are inhaled into the lungs

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77
Q

what happens when someone is infected with TB

A
  • the bacteria are taken up by a phagocyte which is a type of white blood cell
  • replicates inside the phagocytes
  • the immune system seals off the infected phagocytes in structures in the lungs called tubercles so people dont develop TB straight away
  • when sealed inside the tubercles the bacteria become dormant and infected person shows no obvious symptoms
  • later, the dormant bacteria may become reactivated and overcome the immune system which causes TB
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78
Q

who is reactivation of TB more likely in

A

people with weakened immune system

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79
Q

what are the initial symptoms of TB

A
  • fever
  • general weakness
  • severe coughing
  • inflammation
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80
Q

what happens as TB progresses

A
  • as TB progresses it damages the lungs
    • if left untreated it can cause respiratory failure →can lead to death
  • TB can also spread to other parts of the body
    • if left untreated it can cause organ failure which can lead to death
81
Q

how can pathogens enter the body

A
  • cuts in the skin
  • digestive system via contaminated foods or drink
  • the respiratory system
  • through mucosal surfaces e.g mouth, genitals
82
Q

what are the barriers that prevent infection

A

skin
gut + skin flora
stomach acid
lysozyme

83
Q

how does skin act as a barrier to infection

A
  • acts as a physical barrier to pathogens
  • pathogens on the surface can enter your bloodstream
  • blood clots in the area of damage prevent pathogens from entering
  • however some may still get in before the clot forms
84
Q

how does stomach acid act as a barrier to infection

A
  • if you eat or drink something that may contains pathogens, most will be killed by acidic conditions of the stomach
  • some may survive and pass into the intestines where they can invade cells of the gut wall and cause disease
85
Q

how does gut and skin flora act as a barrier to infection

A
  • intestines and skin is naturally covered in flora (which are harmless microorganisms)
  • they compete with pathogens for nutrients and space
  • this limits the number of pathogens living in the gut and on skin
  • makes it harder for them to infect the body
86
Q

how does lysozyme act as a barrier to infection

A
  • mucosal surfaces produce secretions
  • contains lysozyme
  • this kills bacteria by damaging their cell walls and makes the bacteria burst open
87
Q

what are antigens

A
  • molecules found on the surface of cells
  • they are recognised as foreign when a pathogen enters the body
    • found on the surface of pathogens
  • this activates cells in the immune system
88
Q

what does the non specific immune response do

A
  • this occurs first
  • happens in the same way for all microorganisms regardless of which antigen they have
    • not antigen specific
  • starts attacking microorganisms straight away
89
Q

recall the three mechanisms that are a part of the non specific immune response

A

inflammation at the site of infection
production of anti-viral proteins called interferons
Phagocytosis and lysozyme

90
Q

How does inflammation occur

A
  1. inflammation at the site of infection
    - site where a pathogen enters the body is known as the site of infection
    - usually becomes red, swollen, warm, painful which is known as inflammation
    • immune system cells recognise foreign antigens and release molecules that trigger inflammation
    • these cause vasodilation (when the blood vessels widen) at the sight of infection which increases the blood flow to it
    • they also increase permeability of blood vessels
    • increased blood flow brings immune system cells to the site of infection. increased permeability allows the cells to move out of the blood vessels and into the infected tissue
    • immune system cells can then start to destroy the pathogens
91
Q

what do interferons do

A
  • when cells are infected with virus they produce proteins called interferons
  • they help prevent viruses spreading to uninfected cells
  • they do this in several ways:
    • prevent viral replication by inhibiting production of viral proteins
    • activate cells involved in specific immune response
    • also activate other mechanisms in the non specific immune response
92
Q

what is a phagocyte

A
  • a phagocyte is a type of white blood cell that carries out phagocytosis
    • phagocyte is also known as a macrophage
93
Q

what is phagocytosis

A

engulfment of pathogens

94
Q

what is the role of phagocytes and lysozymes in the non specific immune response

A
  • a phagocyte recognises the antigen a pathogen
  • cytoplasm of the phagocyte moves around the pathogen and engulfs it
  • pathogen is now contained in a phagocytic vacuole in the cytoplasm of the phagocyte
  • a lysosome (which contains digestive enzyme) fuses with the phagocytic vacuole and the enzymes break down the pathogen
  • the phagocyte then presents the pathogens pathogens antigens and sticks the antigen on its surface to activate other immune system cells
    • also called an antigen presenting cell
95
Q

How can one gene give rise to more than one protein through post transcriptional changes to mRNA

A

Due to different combinations of exons

96
Q

when would the specific immune response occur

A
  • specific immune response occurs if the pathogen escapes the non-specific immune response
  • an invading pathogen will activate the non specific and specific immune system
97
Q

what are the 2 types of lymphocytes and what do they do

A
  • B- cells attack invaders outside of the cell
  • T-cells attack invaders inside of cells
98
Q

what are b lymphocytes

A
  • mature in bone marrow
  • associated with humoral immunity involving antibodies
  • humoral immunity- extracellular bacteria
99
Q

what are T lymphocytes

A
  • mature in the thymus gland
  • associated with cell-mediated immunity in body cells
  • cell-mediated immunity- viruses and intercellular bacteria
100
Q

what can B lymphocytes develop into

A

plasma and B memory cells

101
Q

what do plasma cells do

A

circulate in the blood and manufacture and release antibodies

102
Q

what do B memory cells do

A
  • remain in the body for a number of years and act as the immunological memory
    • body can recover quicker from infections that theyve been exposed to before because of this
103
Q

what do lymphocytes respond to

A
  • organisms own cells that have been infected by non-self material from a different species
  • other cells of the same species as they are genetically different and so display different antigens
  • cancer cells or transplanted cells as they display different antigens
104
Q

what do T lymphocytes respond to/ how do they work

A

T lymphocytes will only respond to antigens that are presented on a body cell rather than antigens within the body fluids
- they are covered in receptors which bind to antigens
- the receptors on a T cell respond to a single antigen
- therefore there are a vast number of T cells which each respond to a different antigen

105
Q

what are the types of T cells

A

T killer
T helper
T memory

106
Q

what do T helper cells do

A

releases cytokines which are chemical messengers that stimulate B cells and T killer cells to develop
- also stimulates phagocytes and phagocytosis

107
Q

what do T killer cells do

A
  • kill abnormal cells that are infected by pathogens
  • produce perforin which is a protein that makes holes in the cell surface
  • holes makes the cell surface membrane freely permeable which causes the cell to die
108
Q

what do T memory cells do

A

provide long term immunity

109
Q

what does humoral immunity involve

A

for bacteria (outside of the cell- bacteria that doesn’t infect the cell)

  • involves B lymphocytes and antibodies
  • antibodies are soluble in body fluids such as blood
  • there are many B cells and each produces a specific antibody in response to a specific antigen
  • this B cell will have receptors that are complementary to each other
110
Q

what is intracellular bacteria

A

are bacteria, which have the capability to enter and survive in the cells of the host organism

111
Q

what is extracellular bacteria

A

a bacterial pathogen that can grow and reproduce freely, and may move extensively within the tissues of the body

112
Q

recall the process of the humoral immune response

A
  1. macrophages engulf the bacteria, the macrophages present antigens on its surface and become antigen presenting cells to the T helper cells
  2. the CD4 receptors of the T helper cells bind to the antigen and become activated.
    1. the T helper cells release cytokines for B cell activation and stimulation
  3. The B cells divide to form clones of B effector and B memory cells
  4. the process of B cell division is called clonal selection
  5. the B effector cells differentiate into plasma cells
    1. the plasma cells can then secrete antibodies which bind to antigens
  6. the antibodies cause agglutination of the bacteria which facilitates phagocytosis
    . agglutination → clumps bacteria together which makes it easier for phagocytes to engulf it
  7. antibodies can also neutralise toxins
  8. the B memory cells remain for months/years in the body which means that if an individual is exposed to the same antigen in the future their immune system can respond more quickly
113
Q

recall the process for cell mediated respnse

A
  1. macrophage engulfs the bacteria/ virus, the macrophages present antigens on its surface and becomes antigen-presenting cells to the T helper cell
  2. the CD4 receptors on the T helper cells bind to the APC and become activated
  3. the infected host cells present the antigens to T killer cells. The host cell becomes an antigen-presenting cell (APC)
  4. the T killer with the complimentary receptor binds to the APC
  5. cytokines from the T helper cells stimulate the differentiation and clonal expansion of the T killer cells; there are now clones of the active T killer cells and clones of the T killer memory cells
  6. the active T killer cells bind to the infected cells that are presenting antigens
    1. the T killer cells cause lysis of the infected cells
  7. the T memory cell remains for months or years in the body. this means that if an individual is exposed to the same antigen in the future their immune system can respond more quickly
114
Q

what are the 2 types of immunity

A

active and passive

115
Q

what is immunity

A

immune system makes its own antibodies after being stimulated by antigens that have entered the body either naturally or artificially

116
Q

what is passive immunity

A

uses antibodies made by another organism either naturally or artificially

117
Q

what does active immunity involve

A
  • exposure to pathogen
  • pathogen invades the body
    • direct contact with pathogen is needed
  • lag phase before protection develops
  • long term protection
  • memory cells produced
118
Q

what does passive immunity involve

A
  • no immune response
  • antibodies not made by the body→ come from another source
  • no exposure to pathogen/antigen
    • no direct contact with the pathogen is needed
  • immediate protection
  • short-term protection
    • no lasting immunity
  • no memory cells produced
119
Q

what is natural passive immuniy

A
  • transfer of maternal antibodies to the foetus via milk or through placenta
    • the amount and type of antibodies passed onto the baby depends on the mothers immunity
    • immunity in newborn babies is only temporary + starts to decrease after the first few weeks/months
    • breast milk contains antibodies which means that babies who were breastfed have passive immunity for longer
120
Q

what is colostrum

A

colostrum (thick, yellowish milk) produced for the first few days following birth is rich in antibodies

121
Q

why are premature babies at a higher risk at developing an illness

A

their immune systems arent as strong and haven’t had as many antibodies passed to them

122
Q

what is natural active immunity

A

antigens enter the body naturally + the body produces antibodies and specialised lymphocytes

123
Q

what is artificial active immunity

A
  • antigens are introduced in vaccines
  • body produced antibodies and specialised lymphocytes
124
Q

what is artificial passive immunity

A

administration of pre-formed antibodies, tetanus injection, rabies injection, anti-venom antibodies

125
Q

what are the characteristics of artificial passive immunity

A
  • temporary
  • requires the repeated administration of serum containing the antibodies
  • immediate protection
  • no memory lymphocytes produced
126
Q

what can vaccines contain

A
  • attenuated viruses
  • dead bacteria
  • toxin that has been altered into a harmless form
  • an antigen-bearing fragment of the pathogen
    • isolated antigens such as cell surface proteins from the pathogen
127
Q

what are attenuated viruses

A
  • viruses that have been weakened so that they are harmless
    • killed by heat treatment which leaves the immune-stimulating antigens intact
128
Q

how do vaccines work

A
  • induces an immune response in an individual without causing symptoms
  • the body reacts as if its infected and so produced antibodies and memory cells
  • if infected with the same pathogen again→ antibodies are produced much faster
129
Q

what is herd vaccination

A
  • vaccinate most/all people
    • stops infection from spreading within the population
130
Q

what is ring vaccination

A
  • vaccinate all people around the victim
    • contains spread within the ring
    • stops transmission → trace and isolate contacts, travel restrictions
131
Q

how do vaccines induce an immune response

A
  • vaccines contain antigens that stimulate the primary immune response against a particular pathogen
  • the antigen-presenting cells will activate the T helper cells
  • the T helper cells secrete cytokines which activate the B cells and T killer cells
  • the B cells can then differentiate into plasma cells which secrete antibodies
  • the B cells also differentiate into memory cells
  • if the person gets infected with the pathogen again, the antibodies will be produced a lot faster
  • this secondary immune response will get rid of the pathogen before the patient would show any symptoms
132
Q

what are the differences between active and passive immunity

A
  • active involves exposure to antigens whereas passive immunity doesn’t involve exposure to antigen
  • active immunity takes a while to develop immunity whereas in passive immunity protection is immediate
  • in active immunity, protection is long term whereas in passive immunity protection is short term
  • in active immunity memory cells are produced whereas in passive immunity memory cells aren’t produced
133
Q

why are antibodies produced more quickly after the second infection

A

Memory cells remain in greater numbers than the initial B cells, allowing the body to quickly respond to the second exposure of that antigen which is why antibodies are produced more quickly after the second infection than the first

134
Q

what are the pros of vaccination

A
  • highly effective as one vaccination can give lifetime protection
  • however less effective ones will require booster
  • generally harmless as they do not cause the disease they protect against as the pathogen is killed by the primary immune response
135
Q

what are the cons of vaccination

A
  • people can have a poor response e.g if they are malnourished and cant produce the antibodies
  • people may have allergic reactions
  • antigenic variation→ the variation (due to major changes) in the antigens of pathogens causes the vaccines to not trigger an immune response which makes it difficult to produce vaccines that would prompt the immune system quick enough
    • antigens displayed on the virus change due to mutation which makes it hard to immunize a patient against a virus
  • antigenic concealment
136
Q

what is antigenic concealment

A
  • this occurs when the pathogen hides from the immune system by living inside cells
    • or when the pathogen coats their bodies in host proteins or by parasiting immune cells such as macrophage and T cells
    • or by remaining in parts of the body that are difficult for vaccines to reach
137
Q

what is the adv and disadv of live weakened vaccines

A

advantage of live weakened vaccines
- produces a strong immune response so can provide a life-long immunity with 1-2 doses

disadvantages of live weakened vaccines
- not safe for people with compromised immune systems
- need refrigeration to stay potent

138
Q

what are the adv and disadv of inactive vaccines

A

advantage of inactivated or killed vaccines
- safe for people with the compromised immune systems
- easily stored and transported
- doesn’t require refrigeration

disadvantages of inactivated or killed vaccines
- usually require booster shots every few years to remain effective

139
Q

what is the adv and disadv of subunit vaccines

A

advantages of subunit vaccines
- lower chances of adverse reaction

disadvantages of subunit vaccines
research can time-consuming and difficult

140
Q

what is the adv and disadv of conjugate vaccines

A

advantages of conjugate vaccines
- safe for people with immune-compromised systems
disadvantages of conjugate vaccines
- usually requires booster shots every few years to remain effective

141
Q

what is herd immunity

A

resistance to the spread of an infectious disease within a population that is based on pre-existing immunity of a high proportion of individuals as a result of previous infection or vaccination

142
Q

how can you evaluate the use of vaccines

A
  • vaccines have saved millions of lives
  • vaccine production requires the use of animals
  • vaccines have side effects that could cause long term harm
  • vaccines need to be tested on humans → who should be tested, how should trials be carried out and who accepts the responsibility?
  • is it acceptable to trial a new vaccine with unknown health risks
  • should vaccine be made compulsory? since vaccines need to be used on the majority of individuals of a population
143
Q

what happens in the primary response to an antigen

A
  • when a pathogen enters the body for the first time the antigens on its surface activate the immune system
  • non-specific immune response is activated first which then the specific immune response → both make up the primary response
  • eventually the body will produce enough of the right antibody to overcome the infection but during this time the person will show symptoms of the disease
  • after being exposed to an antigen both T and B cells produce memory cells which remain in the body for a long time
144
Q

what do T memory cells do in the primary response

A

T memory cells remember the specific antigen and will recognise it if you encounter the pathogen again

145
Q

what do B memory cells do in the primary response

A

B memory cells record the specific antibodies needed to bind to the antigen

146
Q

what happens in the secondary response

A
  • the person is now immune and their immune system has the ability to respond quickly to a second infection
  • if the same pathogen enters the body again the immune system will produce a quicker, stronger immune response→ this is the secondary response
  • T memory cells divide into the correct type of T cells to kill the cell carrying the antigen
  • B memory cells divide into plasma cells that produce the right antibody to the antigen
  • secondary response gets rid of the pathogen before you show any symptoms
147
Q

what are antibodies

A
  • antibodies are proteins that can stimulate an immune response
    • known as Immunoglobins
148
Q

how do antibodies work

A
  • specific antibodies react with an antigen on the non-self material
  • any molecule could act as an antigen however they are mainly proteins in the plasma membrane of the pathogen
  • antibodies have a specific binding site that binds to the antigen
149
Q

what is the general function of antibodies

A
  • antibodies do to directly destroy antigens
  • antibodies prepare the pathogen for destruction
150
Q

what is the function of antibodies when it comes to bacteria

A
  • antibodies cause agglutination of the bacterial cells
  • this form clumps bacteria making it easier for phagocyte to locate them
  • antibodies serve as markers that simulate phagocytes to engulf the bacterial cells to which they are attached
151
Q

draw the general structure of an antibody and label the parts

A
152
Q

describe the structure of an antibody

A

hinge regions allows flexibility so that the molecule can grip more than one antigen
- they are Y shaped and have two regions
- a variable region
- a constant region
- variable region→ has a shape specific to the shape of the antigen
- constant regions are the same in all antibodies

153
Q

what is the variable and constant regions in antibodies

A
  • variable region→ has a shape specific to the shape of the antigen
  • constant regions are the same in all antibodies
154
Q

is using body temperature useful in determining time of death

A
  • useful because time of death an be calculate if ambient temp is known
  • only useful for a short period of time following death
155
Q

how is carbon dioxide and ammonia formed during putrefaction in decomposition

A
  • microorganisms respire anaerobically
  • converts organic compounds to CO2
  • converts nitrogen compounds such as proteins to amino acids
156
Q

how do decomposers recycle carbon

A
  • carbon compounds in plant material
  • digestion provides respiratory substrates
  • carbon dioxide released from respiration
  • this carbon dioxide is available for photosynthesis
157
Q

how doe HIV infect T helper cells

A
  1. sticking through the envelope are large glycoprotein molecules, for example gp120 which are specific to the virus. the gp120 molecules bind to CD4
  2. receptor molecules on the host cells surface. there is a second molecule on the cell surface CCR5 which is a receptor the virus attaches to enabling it to enter the host cell as the membranes fuse
  3. when the viral envelope has fused with the cell surface membrane, the contents of the virus particle can enter the cell. the viral genetic material consists of RNA.
  4. to turn this into DNA, reverse transcription has to take place. for this, the virus uses an enzyme called reverse transcriptase.
  5. the DNA produced is then inserted into the hosts DNA and using another virus enzyme called integrase, like any other set of genes, producing proteins and other components for new virus particles
  6. when the new virus particles have been assembled they bud out of the host cell, taking an envelope of cell membrane on the way out.
  7. this causes death of the host cell, which damages the immune system of the infected person because the virus infects T helper cells, important for fighting disease.
  8. as HIV is currently incurable the patient will eventually develop AIDS
158
Q

what is the HIV envelope made from

A

HIV is an example of an enveloped virus. the envelope is made from lipid bilayer and this is derived from the host cells cell membrane when the new virus emerges from the cell

159
Q

how can clinical trials of a vaccine be conducted

A

vaccine is first tested on healthy volunteers to test for side effects
health volunteers tested for presence of antibodies to the virus
group of people at risk of contracting the disease is given the vaccine
the number of people who develop the viral diseases after the vaccnation are monitored

160
Q

how can you justify the use of vaccine even though clinical trials have not been completed on patients and health workers

A

stops the spread of the disease
large numbers of people have died from the disease
health workers are in close contact with people have died from the disease
the side effects of the vaccine will not be worse than contracting ebola
if health workers were vaccinated they could care for more people

161
Q

how do vaccines work against viruses

A

T helper cells bind to antigen on the APC
therefore leading to the production of active T helper and T memory cells
the T helper cells activate the B cells to become B effector cells and and then plasma cells which are capable of producing antibodies
the memory cells remain in the body so antibodies can be produced quickly on re-infection

162
Q

why does the destruction of T helper cells cause the symptoms of AIDS

A

lack of cytokines reduces cytokine production
therefore reducing activation of B cells which reduces antibody production
could lead to opportunistic infection

163
Q

how can stem cells be used to prevent HIV from causing AIDS

A

stem cells form the bone marrow can differentiate into specialised cells
the stem cells will differentiate into T helper cells that are resistant to HIV
T helper cells are destroyed by HIV so the patient cannot produce an immune response
mutated CD4 receptor prevents HIV entering the replacement T helper cells
T helper cells are not destroyed therefore HIV is not present in the blood

164
Q

Explain why the presence of microorganisms on the skin and in the gut helps to prevent pathogenic organisms multiplying in the body

A

Flora in the gut and skin are better adapted to the conditions
Therefore they can outcompete pathogenic organisms
Bacteria in the gut secrete chemicals which help to destroy pathogens

165
Q

explain why the presence of microorganisms on the skin and in the gut helps to prevent pathogenic organisms multiplying in the body

A

flora in the gut are better adapted to the conditions
they can outcompete pathogenic organisms
bacteria in the gut secrete lactic acid which help to destroy pathogens

166
Q

why is the primary immune response slow

A

primary response is slow as there arent many B cells that can make the antibody needed to bind to the antigen

167
Q

what study can be carried out to study the changes in insect species on a body (e.g animal) after death

A

standardisation of animal studied e.g same mas, age, sex, size
control temperature, humidity/ abiotic factors
record the presence of different species of insects at regular time intervals

168
Q

how can the results of an investigaion used to study the changes in insects on a body help establish the time of death

A

record insects present on the human body and compare it to the results from the investigation to determine time of death
take into account stages of the lifecycle of insects that are present
when using stage of succession to determine time of death take into account environmental factors

169
Q

what are antiretroviral drugs

A

no treatment to get rid of HIV as the virus is hidden inside T helper cells
drugs that can reduce the production of more viruses

170
Q

recall the type main types of antiretroviral drugs

A

reverse transcriptase inhibitors
protease inhibitors

171
Q

what does reverse transcriptase inhibitors do

A

prevent viral RNA from making DNA for integration into the hosts genome

172
Q

what does protease inhibitors do

A

inhibit the proteases that catalyse the curing of larger proteins into small polypeptides for use in the construction of new viruses

173
Q

why are antiretroviral drugs often given in combination

A
  • HIV can develop resistance to anti-HIV drugs and therefore these drugs are often given in combination
  • if the virus becomes resistant to one drug it may still be susceptible to the other drugs being taken
174
Q

why is there a decline in the number of AIDS-related deaths

A

access to antiretroviral is increasing across the world and with it comes to a decline in the number of AIDS-related deaths `

175
Q

what was the first ever antibiotic discovered and by who. what is its effect on TB

A

alexander fleming
penicillin
no effect on the bacteria that causes TB

176
Q

what was the first drug found that could cure TB

A

streptomycin

177
Q

what is waksman definition of antibiotics

A

a chemical substance, produced by microorganisms which has the capacity to inhibit the growth and even to destroy bacteria and other microorganisms in dilute solutions

178
Q

why do some microorganisms make antibiotics

A
  • usual answer is that antibiotics help microorganisms to compete in the environment
  • however if this was the case it would be expected that the antibiotics would be produced mainly in young cells but instead, they are not produced in large amounts until the cells are ageing
179
Q

what are the features of antibiotics

A

→ they are effective against bacterial cells but leave eukaryotic cells unharmed

→ they are useless against viruses so diseases such as colds and flu should not be treated with antibiotics

180
Q

how can TB be treated

A
  • antibiotics can kill active TB bacteria
  • a combination of four antibiotic drugs is given for two months
  • then two drugs are used for a further 4 months which ensures that any dormant bacteria is destroyed
181
Q

what are the two classes of antibiotics

A

bactericidal
bacteriostatic

182
Q

what do bactericidal antibiotics do

A

destroy bacteria by inhibiting cell wall synthesis, RNA and DNA synthesis

183
Q

what do bacteriostatic antibiotics do

A

prevent the multiplication of bacteria without directly killing the bacteria
the hosts own immune system can then destroy the pathogens

184
Q

how do bactericidal antibiotics disrupt cell growth and division

A
  • inhibition of bacterial cell wall synthesis → if a weak wall forms this can lead to lysis (bursting) of the cell
  • disruption of the cell membrane → causing changes in permeability that lead to cell lysis
  • inhibition of nucleic acid synthesis, replication and transcription → prevents cell division and/or synthesis of enzymes
  • inhibition of protein synthesis, meaning enzymes and other essential proteins arent produced
  • inhibition of specific enzymes found in the bacterial cell but not in the host
185
Q

why are diseases such as TB still around

A
  • the selective pressure exerted by the pathogens have resulted in the human genome which makes us more resistant
  • pathogens and hosts are locked in an evolutionary arms race which is why people are still dying of diseases that have been around for centuries
186
Q

what is an evolutionary arms race

A

this is when as quickly we evolve mechanisms to combat pathogens, the pathogens evolve new methods of overcoming our immune system

187
Q

why may pathogens have an advantage in the evolutionary arms race

A
  • bacteria reproduce very quickly
  • bacterial populations are usually in billions so the number of cells containing mutations is vast
  • some of these random mutations will be advantageous to the cell containing them
    bacteria with a useful mutation are more likely to survive, reproduce and spread
188
Q

what random mutations could be advantageous to the cell containing the pathogen

A

they may allow the cell to use different food resources
reproduce more quickly
infect other cells more successfully
produce symptoms in the host such as coughing and sneezing which aid the spread of the disease

189
Q

what are the evolution bacterial strategies for evading or disabling the immune system

A

e.g a slight change in the antigen of the pathogen means that the antibodies, B and T memory cells from a previous infections wont work in a second infection

190
Q

how can antibiotics act as a selection pressure

A

mutations arise in the pathogenic bacteria can make them resistant to antibiotics

191
Q

how can bacteria mutate to make them resistant to antibiotics

A

the bacteria may produce an enzyme which enables them to break down the antibiotic or use a different metabolic pathway for the reactions inhibited by the antibiotic
- the bacteria that dont possess the gene for resistance are more likely to be destroyed → they are selected against
- those that have the gene would survive, grow and reproduce → they are selected for

192
Q

in the absence of the antibiotic why may bacteria with the mutation be at a disadvantage

A

they may reproduce more slowly as they may be using resources to produce enzymes that under normal circumstances arent required

193
Q

what is vertical evolution

A

the advantageous gene is passed vertically from one generation to the next is sometimes called vertical evolution

194
Q

what is horizontal evolution

A
  • this is when the gene is passed on from one bacterium to another
    • maybe the same or different bacterial species
      bacteria dont undergo sexual reproduction but they do have cell-to-cell contact in a process called conjugation
195
Q

describe how conjugation occurs

A

plasmid carrying gene for antibiotic resistance is in resistant bacterial cell
one strand of plasmid DNA transfers between conjugating bacteria (transferred to non resistant bacteria)
both bacteria is now resistant

196
Q

why would resistant bacteria be at an advantage in the presence of the antibiotic

A

they will survive and reproduce more rapidly as there will be less competition
this explains why some people with the disease may appear to improve at first in response to a single drug and then worsen as the drug-resistant mutants multiply unchecked

197
Q

why wasnt antibiotic resistance a problem for many years

A

this wasn’t a problem because new antibiotics were being developed faster than the bacteria developed resistance
however the bacteria are catching up, with fewer new drugs being successfully developed

198
Q

why have hospitals tightened their infection control

A
  • some bacteria have evolved resistance to several antibiotics
  • these bacteria are common in hospitals and are creating problems for the treatment of infected patients
  • in response to the increased number of patients becoming infected with healthcare-associated infections (HCAI)
199
Q

what practices have hospitals put in place to stop the spread of infection

A
  • hand washed at the entrance to every ward
  • signs reminding all hospital personnel to wash their hands
  • rules preventing doctors and nurses wearing ties, watches or long sleeves
  • antibiotics only used when the patient has definitely been diagnosed as suffering from a bacterial infection
  • patients are now advised to complete the whole course of their antibiotics even when they feel better so that all the bacteria is destroyed
  • better professional and public education on the problem of antibiotic resistance
200
Q

why did some doctors prescribe antibiotics even when suffering from a viral infection

A

because the patient expected it or just incase

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