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Unit 4 Revision Notes.: Topic 5 Summary
Unit 4 Revision Notes.: Topic 5 Summary
Unit 4 Revision Notes.: Topic 5 Summary
These notes do not cover absolutely everything, but they do cover those major topics and the wording you
seem to have the greatest difficulty with.
Check the Specification and the ‘Check Your Notes’ summary.
TOPIC 5
Topic 5 summary
Make sure your notes cover the following points. The points are listed in the approximate order they appear
within the topic. All the points are covered in the textbook but where there is supporting information within
the activities this is indicated.
There are suggestions on making notes and on revision in the Exam/coursework support.
You should be able to:
o Explain that the numbers and distribution of organisms in a habitat are controlled by biotic and abiotic
factors. (Activity 5.1 and 5.2) (Checkpoint question 5.4)
o Explain how the concept of niche accounts for distribution and abundance of organisms in a habitat.
(Activity 5.1 and 5.2) (Checkpoint question 5.1)
o Describe how to carry out a study on the ecology of a habitat to produce valid and reliable data
(including the use of quadrats and transects to assess abundance and distribution of organisms and the
measurement of abiotic factors, e.g. solar energy input, climate, topography, oxygen availability and
edaphic factors). (Activity 5.2)
o Describe the concept of succession to a climax community. (Activity 5.3) (Checkpoint question 5.2)
o Describe the overall reaction of photosynthesis as requiring energy from light to split apart the strong
bonds in water molecules, storing the hydrogen in a fuel (glucose) by combining it with carbon dioxide
and releasing oxygen into the atmosphere. (Activity 5.4 and 5.5) (Checkpoint question 5.3)
o Describe how phosphorylation of ADP requires energy and how hydrolysis of ATP provides an
immediate supply of energy for biological processes. (Activity 5.4 and 5.5)
o Describe the light-dependent reactions of photosynthesis including how light energy is trapped by
exciting electrons in chlorophyll and the role of these electrons in generating ATP and reducing NADP
in photophosphorylation and producing oxygen through photolysis of water. (Activity 5.4 and 5.5)
o Describe the light-independent reactions as reduction of carbon dioxide using the products of the light-
dependent reactions (carbon fixation in the Calvin cycle, the role of GP, GALP, RuBP and RUBISCO)
and describe the products as simple sugars that are used by plants, animals and other organisms in
respiration and the synthesis of new biological molecules (including polysaccharides, amino acids, lipids
and nucleic acids). (Activity 5.4, 5.5 and 5.6)
o Describe the structure of chloroplasts in relation to their role in photosynthesis. (Activity 5.4)
o Carry out calculations of net primary productivity and explain the relationship between gross primary
productivity, net primary productivity and plant respiration. (Activity 5.8)
o Calculate the efficiency of energy transfers between trophic levels. (Activity 5.8)
o Analyse and interpret different types of evidence for global warming and its causes (including records of
carbon dioxide levels, temperature records, pollen in peat bogs and dendrochronology) recognising
correlations and causal relationships. (Activity 5.9, 5.10 and 5.11)
o Outline the causes of global warming – including the role of greenhouse gases (carbon dioxide and
methane, CH4) in the greenhouse effect. (Activity 5.12 and 5.13)
o Discuss the way in which scientific conclusions about controversial issues, such as what actions should
be taken to reduce global warming or the degree to which humans are affecting global warming, can
sometimes depend on who is reaching the conclusions. (Activity 5.14 and 5.15)
o Describe how data can be extrapolated to make predictions, that these are used in models of future global
warming, and that these models have limitations. (Activity 5.16)
o Describe the effects of global warming (rising temperature, changing rainfall patterns and changes in
seasonal cycles) on plants and animals (distribution of species, development and life cycles). (Activity
5.17 and 5.21) (Checkpoint question 5.5)
o Explain the effect of increasing temperature on the rate of enzyme activity in plants, animals and micro-
organisms. (Activity 5.18)
o Describe how to investigate the effects of temperature on the development of organisms (e.g. seedling
growth rate, brine shrimp hatch rates). (Activity 5.19 and 5.20)
o Describe how evolution (a change in the allele frequency) can come about through gene mutation and
natural selection. (Checkpoint question 5.6)
o Describe the role of the scientific community in validating new evidence (including molecular biology,
e.g. DNA, proteomics) supporting the accepted scientific theory of evolution (scientific journals, the peer
review process, scientific conferences). (Activity 5.22 and 5.23)
o Discuss how understanding the carbon cycle can lead to methods to reduce atmospheric levels of carbon
dioxide (including the use of biofuels and reforestation). (Activity 5.25) (Checkpoint question 5.7)
Demonstrate knowledge and understanding of the How Science Works areas listed in the table on page 13 of
the specification
Topic 5
Biotic and abiotic factors affect the distribution and abundance of species in a habitat
When these factors are favourable organisms survive, grow and reproduce successfully. When
these conditions are unfavourable, organisms don’t survive, grow or reproduce as successfully.
Be prepared to answer questions on organisms and habitats you have not seen before; the
question and any data should give you sufficient information to be able to interpret the factors,
both biotic and abiotic, affecting the distribution (i.e. where the species lives in the habitat) or
abundance (how many there are per unit area) of the organisms in question. Do not be afraid to
think and come up with biologically sensible ideas!
The distribution and abundance of any species varies because of the abiotic factors e.g.
amount of light or temperature, and the biotic factors e.g. preadators, parasites, competition for
food. When these factors are favourable organisms survive, grow and reproduce successfully.
When these conditions are unfavourable, organisms don’t survive, grow or reproduce as
successfully.
In any habitat it is clearly impossible to count all the organisms so we need to take a
representative sample i.e. a sample within which the numbers of the different organisms or
species is representative of the whole area i.e. in the same proportions.
Sampling strategies
Sampling strategies
• In a uniform environment random
sampling is used
• Quadrats are placed at random to avoid
bias
X
X
X
X
How?
B Divide the area into a grid (e.g. using
measuring tapes, string with knots in at 1m
intervals)
1 2 3 4 ogenerate random numbers – e.g. use
1 random number generator on a calculator,
dice, random number tables – these give
2 the coordinates of a random quadrat;
oin this example A3, B2 defines the top
A
3 X left hand corner of the shaded quadrat on
the diagram
4 orepeat the procedure for the number of
quadrats to be taken.
5 oplace the each quadrat on its appropriate
coordinates.
oin each quadrat count the number of
organisms of the species under
investigation.
This produces a valid representative sample.
This allows us to estimate the abundance (i.e. how many) of species in a particular area.
In a non-uniform environment where conditions change across a habitat (e.g. on the sea shore
between the low and high water marks) random sampling is not always appropriate. In this case
quadrats are placed systematically (i.e. in a sequence
X x x x
X or
X x x
X
X x x x
A line transect down a slope,
across a rocky shore Around a pond
Investigation of the biotic and abiotic factors affect the distribution and abundance of
species in a habitat
e.g. Investigation of the distribution and abundance of heathers on the heathland
Line transect top to bottom of slope/sample every 5 m/ 3 random samples chosen using dice –
avoids bias – 0.25m2 quadrat, count number of each of 3 species of heather in the 100 small
squares to estimate frequency/soil samples to determine % moisture/plot data on kite diagram.
Erica cinerea only found in dry soil, Erica tetralix found only where soil is wet
Succession
Succession is the progressive change in the composition and diversity of the species in a
community in one place over a period of time
Primary succession: Starts in new habitats with no soil and no previous community; extreme
environmental conditions: Secondary succession: Starts on bare soil where there had previously
been a community; extreme environmental conditions
Characteristics of all successions
The initial environment is hostile and extreme. First colonisers are called pioneer species
Pioneer plants are highly adapted to withstand hostile conditions
The abiotic factors in this environment mainly determine what species are present since few
species can tolerate such conditions so in the initial stages the biodiversity will be low
The initial colonisers modify the environment to make it less extreme
pioneer plants die organic matter incorporated into developing soil/nitrate content of soil
increases
existing plants provide increasing dead organic matter and nitrates so soil develops, they
provide shade and shelter, reduce wind speed to reduce transpiration etc so improve the
environment so more plants now able to establish and grow so early colonisers are
outcompeted by later colonisers (e.g. grasses shade out mosses, trees shade out grasses) so
community changes so more plants can grow so biodiversity increases
As number of different species present increases so there will be more microhabitats for
organisms to exploit/greater variety of food plants for associated organisms/greater variety of
feeding niches so biodiversity of associated animal community will change too
In the latter stages biotic factors largely determine which organisms can survive, e.g.
predation, grazing, competition etc
The stable end point community is characteristic and is called the climax community usually
dominated by trees. It is in equilibrium with the environment so undergoes little it any further
change
Photosynthesis
Photolysis of water
electrons from water are used to replace the electrons lost from the chlorophyll
these are then excited when the chlorophyll absorbs light to be used to make more ATP as
before
oxygen is the valuable waste product of photolysis
Light independent stage
Trophic levels
Primary producers
Not all the visible light energy coming in from the sun ever reaches a plant
Some is reflected by clouds and dust
Some will miss the leaves altogether
Some is not of the right wavelength to be absorbed by the photosynthetic pigments
which absorb blue and red but not green
Some of this is then lost as heat by the reactions of p/s
What is left is fixed in the organic molecules which are the products of p/s; this
the gross primary productivity
Gross primary productivity = the amount of energy fixed in the sugars etc. produced
by the chloroplasts by p/s
Much of the sugars produced are immediately broken down in respiration to provide the energy
for the metabolic reactions of the cells. The remaining sugars are converted into starch,
cellulose, etc in the cells of the plant
becoming new biomass.
In general less than 10% of the energy in the food taken in ends up in the biomass
As a consequence of the use of energy and losses of energy at each trophic level, less
energy is transferred to each successive level so the amount of energy in each
successive level decreases.
This ultimately limits the number of trophic levels. So much energy is lost between levels that
final level contains so little energy that, if only 10% of this is transferred there simply isn’t enough
to support any further biomass.
The amount of energy available decreases in successive trophic levels so the amount
of biomass which can be supported also decreases and this is ultimately reflected in a
general reduction in numbers in successive trophic levels. (this is shown in pyramids of
energy, biomass and numbers)
Natural selection.
All organisms contain DNA which is ‘read’ in the same way, providing evidence of evolution from
a common ancestor.
DNA and proteins contain a record of genetic changes resulting from random mutations over
time, indicating gradual change within and between species. Studying DNA and proteins allows
these changes to be identified.
Genomics (the study of DNA); look at the sequence of bases in genes; the more distantly related
two species are the more differences there will be due to the accumulation of mutations over
time.
In order for new evidence to be accepted as support (or rejection) for the theory of evolution (or
any other theory for that matter) it needs to be regarded as VALID.
Peer review. Before a scientific paper is published is would be sent to a few eminent
experts in the field for a peer review; they would examine the paper critically to check the
validity of the method,(e.g. use of the right controls) the proper use of statistics to analyse the
data and the validity of the conclusions, especially in the light of what other scientists have
found and published.
Publishing the research and its conclusions. The scientific paper is then published in a
reputable scientific journal so the rest of the scientific community are made aware of the
findings. Many of these are now on-line so that important information is so much more
accessible and available faster to a wider audience.
o One of the big problems with use of the Internet is that the peer review process can
be circumvented and poorly conducted research or invalid conclusions could get into
the public domain.
Presentation of papers at scientific conferences Many new findings are also brought to
the attention of other scientists in the field by the presentation of papers at scientific
conferences. Here perceptive questions ensures the author can justify his findings and also
spark new interpretations, new ideas and new lines of research.
The evidence
Provides information back possibly as far as the last Ice Age (circa 12 000 years ago).
Peat formed when plant material dies but does not decompose
The peat accumulates in successive layers; lowest layers are the oldest: pollen trapped in peat
layers
Use of carbon dating techniques can establish the age of the layers
Use of pollen records from peat
Trees produce a ring of new xylem each year = growth ring. Xylem vessels produced in
spring are wider than those produced in the summer and the difference in vessel size from
summer to the next spring is what demarcates the ring.
Outer ring is current year; each ring can be dated by counting inwards
Width of ring reflects amount of xylem produced which reflects amount of growth
Wide ring = lots of growth so by inference climatic conditions favoured growth e.g. warm/wet
So, age of rings and widths provide clues about past climatic conditions
The Earth appears to have been warmer since 1980 than at any time in the last 18 centuries.
The Earth has warmed by 0.5oC over the last century and at least 0.2oC in the last 20 years or so -
the greatest amount by which it has warmed or cooled over the space of a century in the past.
Temperature and other data shows mean global temperature is rising. Fact.
What is causing it? Several possible explanations (i.e. theories)
Greenhouse effect
light energy from the Sun reaches the Earth’s surface and is absorbed so the Earth warms up
some of this energy is radiated back into space as longer wavelength infrared radiation.
the atmosphere contains gases, including carbon dioxide, water vapour and methane, which
absorb some of this infrared radiation so stopping it leaving. These are called greenhouse
gases.
this causes the atmosphere to warm up which in turn warms up the Earth’s surface.
Greenhouse gases absorb infra red radiation: the main greenhouse gases are:
water vapour
carbon dioxide
methane
Enhanced greenhouse effect; increased levels of greenhouse gases, especially CO2 and
methane, result in more heat trapped in the atmosphere leading to global warming
The enhanced greenhouse effect, due to raised CO2 levels, is a theory to possibly explain the fact
that global warming is occurring
i.e. the enhanced greenhouse effect is a possible cause and global warming is the effect
Under normal circumstances the CO2 level will remain constant because the processes which add
CO2 are balanced by the processes that remove CO2 from the atmosphere, i.e. in equilibrium
But the CO2 level will increase if the processes of the carbon cycle become unbalanced.
Combustion
o burning fossil fuels e.g. coal. oil, petrol, natural gas
o burning of trees and tree debris (from felling operations) releases CO2: trees contain a
lot of biomass and are important ‘carbon sinks’ (i.e. CO2 used by p/s as the tree grows
and the carbon atoms are removed from the carbon cycle and ‘locked away’ in the
cellulose and lignin of the wood biomass so a lot of extra carbon will be released by
burning)
Deforestation:
o Loss of trees will result in loss of CO2 uptake by photosynthesis in the short term so
CO2 level will rise
o Increase in decomposition of dead organic matter in soil
loss of forest cover exposes soil to the sun so it warms up so the rate of
activity of the decomposers will increase so releasing more CO2.
Other possible causes of global warming
1. Extrapolation of existing data into the future ‘looks forward’ based on previous data;
Extrapolation is involved extending the line of best fit through existing data into the future.
Assumes: there is enough data to establish the trend accurately/present trends continue, e.g. in
fossil fuel use, no changes in control of emissions
2. Use of computer models to predict possible future changes ‘looks forward’ and makes
predictions based on current knowledge
Models are tested by using previous data and seeing if they match the current reality – allows
for ‘tweaking’ but never will be perfect, but they make the best predictions of trends based on
all the data available.
Predictions may be incorrect because of: (don’t learn all of these – be selective!)
Limited data –accurate records do not go back far enough to produce a reliable trend line -
but bigger datasets are becoming increasingly available e.g. accurate CO2 data only from 1950s,
early temperature measurements inaccurate using mercury or alcohol thermometers
Models assume existing trends will continue (by extrapolation of a trend line which has lots of
fluctuations in it – these are limitations in themselves!)
Limited knowledge of how the global climatic system works so models are only
approximations – but knowledge is increasing all the time; e.g. impact of changing ocean
currents on weather systems
Not all factors included; e.g. effects of increasing cloud cover, decreasing snow cover;
unforeseen factors (e.g. major volcanic events,
changes in solar radiation levels) could upset models too.
Future changes in future changes is usage of fossil fuels or emission controls
Limitations of computing resources – but computer technology is improving all the time
If we accept the CO2 levels are rising and are probably linked to rising global temperatures, what
can be done about it? How could we restore the CO2 balance?
1: Reduce CO2 release (cut the emissions of greenhouse gases) by reducing use of fossil fuels
2: Move towards alternative sources of energy e.g. nuclear power, wind, wave power
3: Use of biofuels (= biomass)
o biofuels are any source of energy produced, directly in plants or indirectly in animals,
by recent photosynthesis]
o they can be any kind of fuel made from living things e.g. wood (e.g. willow biomass), or
from the waste they produce e.g. straw, chicken waste,
o or ethanol (from fermentation of plant biomass ) or methane, (from fermentation of
animal waste, sewage waste), or biofuel oils from plants
o biofuels such as wood are
o ‘carbon neutral’ i.e. they fix CO2 from the atmosphere by p/s to grow, so
burning simply releases this CO2 back into the atmosphere again to be re-used
in photosynthesis by more growing crops.
o since burning a biofuel replaces the CO2 used in its growth there is no net
increase in CO2 levels in the atmosphere.
o In theory at least, using biofuels means less fossil fuels are burned so reducing
CO2 emissions.
Reafforestation:
o Replaces trees
o Young forests grow rapidly – take up CO2 by p/s rapidly (especially if climate is
warmer!) and turn it into biomass (growing new wood) faster than respiration
occurs, so net CO2 absorption occurs
o As trees get bigger carbon taken up and ‘locked away’ in biomass of wood of tree
so forests act as a carbon sink to keep carbon out of the atmosphere (so there is
less CO2 contributing to global warming)
o May slow down further increase in atmospheric CO2 so long as reafforestation is a
continuous process on a large scale worldwide > deforestation
Limitations to reforestation :
o Mature forest has trees which are not growing so becomes carbon neutral [CO2
uptake by p/s = CO2 release by respiration] so benefit only lasts whilst forest grows
o Only a limited amount of land which can be used to grow forests (land needed to
live on, grow food on etc, plus trees don’t grow above the tree line)
A typical question:. Why might relatively small increases in temperature have a large effect on the
survival of particular animals and plants in particular places?
1) Describe how DNA can be amplified using the polymerase chain reaction (PCR). (Activity 6.4)
2) Describe how gel electrophoresis can be used to separate DNA fragments of different length. (Activities
6.1 and 6.2)
3) Describe how DNA profiling is used for identification and determining genetic relationships between
organisms (plants and animals). (Activities 6.3 and 6.5) (Checkpoint question 6.1)
4) Describe how to determine the time of death of a mammal by examining the extent of decomposition,
stage of succession, forensic entomology, body temperature and degree of muscle contraction. (Activity
6.5) (Checkpoint question 6.2)
5) Describe the role of microorganisms in the decomposition of organic matter and the recycling of carbon.
(Checkpoint question 6.2)
6) Distinguish between the structure of bacteria and viruses. (Activity 6.6) (Checkpoint question 6.3)
7) Describe the non-specific responses of the body to infection, including inflammation, lysozyme action,
interferon, and phagocytosis. (Activity 6.7) (Checkpoint question 6.4)
8) Explain the roles of antigens and antibodies in the body’s immune response including the involvement
of plasma cells, macrophages and antigen-presenting cells. (Activity 6.8) (Checkpoint question 6.5)
9) Distinguish between the roles of B cells (including B memory and B effector cells) and T cells (T
helper, T killer and T memory cells) in the body’s immune response. (Activity 6.8) (Checkpoint
question 6.5)
10) Explain how bacterial and viral infectious diseases have a sequence of symptoms that may result in
death, including the diseases caused by Mycobacterium tuberculosis (TB) and Human
Immunodeficiency Virus (HIV). (Activities 6.9, 6.11 and 6.17) (Checkpoint question 6.6)
11) Explain the process of protein synthesis (transcription, translation, messenger RNA, transfer RNA,
ribosomes and the role of start and stop codons) and explain the roles of the template (antisense) DNA
strand in transcription, codons on messenger RNA, anticodons on transfer RNA. (Activities 6.12
and 6.13)
12) Explain the nature of the genetic code (triplet code, non-overlapping and degenerate). (Activity 6.12)
13) Explain how one gene can give rise to more than one protein through post-transcriptional changes to
messenger RNA. (Activity 6.13)
14) Describe the major routes pathogens may take when entering the body and explain the role of barriers in
protecting the body from infection, including the roles of skin, stomach acid, gut and skin flora.
(Activity 6.14)
15) Explain how individuals may develop immunity (natural, artificial, active, passive). (Checkpoint
question 6.7)
16) Describe how to investigate the effect of different antibiotics on bacteria. (Activity 6.15)
17) Distinguish between bacteriostatic and bactericidal antibiotics. (Activity 6.16)
18) Discuss how the theory of an ‘evolutionary race’ between pathogens and their hosts is supported by the
evasion mechanisms as shown by Human Immunodeficiency Virus (HIV) and Mycobacterium
tuberculosis (TB). (Activity 6.17)
19) Describe how an understanding of the contributory causes of hospital acquired infections have led to
codes of practice relating to antibiotic prescription and hospital practice relating to infection prevention
and control. (Activity 6.17)
Demonstrate knowledge and understanding of the How Science Works areas listed in the table on page 13 of
the specification.
Table of Contents
Polymerase chain reaction ................................................................................ 18
Producing a DNA profile .................................................................................... 18
Determination of the time of death .................................................................. 19
Causes of decomposition................................................................................... 20
Forensic entomology ......................................................................................... 20
Non-specific responses to infection .................................................................. 22
TB ...................................................................................................................... 24
Antibiotics ........................................................................................................... 25
HIV ................................................................................................................... 27
Nature of genetic code. ..................................................................................... 27
HIV Infection and AIDS .................................................................................................................. 29
Topic 6
How to identify a dead body
Causes of decomposition
Autodigestion or autolysis due to action of hydrolytic enzymes (= self-digestion!) begins about 4
mins after death!
In gut
from lysosomes in cells
Causes breakdown of body tissues
Action of bacteria
From gut especially, later those from outside which invade through natural openings or
wounds,
Initially aerobic bacteria but these use up oxygen so replaced by anaerobic bacteria which
cause putrefaction
Forensic entomolog
This is especially useful when the body has been dead for more than a few days, because the
features that are normally used to determine the time of death, like temperature or rigor mortis,
are no longer helpful
Many types of fly will lay their eggs in a dead body because it is a source of food for the larvae
(maggots). Eggs can be laid on the skin, in body openings, e.g. nose, ears, mouth or in wounds
As the body decomposers it undergoes changes which may make it more attractive to
other species.
The flies etc which feed on the body also bring about changes in it that also make attractive
to other species.
Decomposition follows a predictable sequence, so do the insect species found over time.
Cause of death: structure of bacteria and viruses
Structure of a bacterium
Structure of a virus
Bacteria Viruses
• Prokaryotic cells • No cellular structure
• Cell wall, cell membrane, cytoplasm, no • Protein coat surrounding nucleic acid
organelles, DNA not in a membrane- molecule. May have outer envelope
bound nucleus. May have mucilage derived form host cell
capsule
• Typically 10 mm in size • Typically up to 400 nm in size, so very
(x 25 times bigger) much smaller
• Genetic material is DNA • Genetic material is DNA or RNA
• Reproduce by binary fission (asexual) • Reproduce by inserting nucleic acid into
host cell which ‘reads’ the genes to
synthesise new virus particles which are
released
Defence against disease.
Lysozyme
• Enzyme found in tears, nasal secretions, saliva
• first line of defence against bacteria entering body through eyes, nose or mouth
• breaks down bacterial cell wall
Inflammation
• Damage/infection causes damaged mast cells (cells found in connective tissue) to release
hisamine
• causes vasodilation of the arterioles nearby so more blood flows to area of infection
• also increases permeability of capillaries so more tissue fluid forced out -> localised
swelling
• Phagocytes can squeeze out of capillaries into the tissues to destroy the bacteria to limit
infection.
Phagocytosis
• Non-specific first line of defence mechanism if any pathogens have got into the blood or
tissues
• phagocytes recognise antigens on surface of pathogen as foreign; engulf pathogens
(phagocytosis – a form of endocytosis); killed by hydrogen peroxide produced and digested
by enzymes from lysosomes
Interferon
• Cells infected with virus secrete a protein called interferon (a type of cytokine)
• attaches to membranes of surrounding cells.
• this triggers the cells to make their own antiviral proteins which inhibit synthesis of viral
proteins so no new viruses can be produced, so limiting infection.
• Also stimulates virus-infected cells to ‘self-destruct
Significance
• Interferon system reacts very quickly to viral infection
• This limits the infection until the slower acting specific immune response kicks in to take
over.
Involves B and T lymphocytes in the blood and lymphatic system responding to a specific
pathogen once it has got passed the non-specific lines of defence
Both type of cell respond to specific antigens associated with the pathogen (or foreign tissue)
and this specificity is what makes them part of the specific immune response.
Antibodies do a variety of jobs, including clumping bacterial cells together so they can be
taken in by phagocytes.
• Memory cells from the first infection (primary immune response) enable a much
faster response to occur to a subsequent infection by the same pathogen with the same
antigens.
• Exposure to the antigen results in the B memory cells differentiating into plasma cells;
• Response occurs in 2-7 days (since all the initial activation steps don’t need to happen)
• more cells are produced much faster than in 1o response because the initial antibody
presentation/B cell multiplication phases to produce the memory cells in the first place has
already happened (so the sequence is further along)
This is immunity.
Active immunity
• the body produces antibodies in response to an antigen following infection
• artificially acquired by injection of vaccines containing dead or weakened forms of a pathogen
Passive immunity
• Ready-made antibodies pass from mother across placenta and in milk
• Artificially acquired by injection of serum containing antibodies e.g. anti-venom.
Herd immunity
• Achieved when enough people in a community are immunized against certain diseases so it is
more difficult for that disease to get passed between those who aren't immunized.
TB
Some M. tuberculosis bacteria may survive inside macrophages. The bacteria have
very thick waxy cell walls, making destruction inside the macrophages very
difficult. The bacteria can lie dormant for years.
The second phase (active tuberculosis) occurs if there are too many bacteria for the
immune response to deal with, or if an old infection breaks out because the
immune system is not working properly.
The lung damage will eventually kill the sufferer if they are
not treated with an appropriate antibiotic.
Active TB
the number of bacteria increases producing more tubercules and severely damaging the lung
tissue leading to break down of alveoli, producing large cavities
these severely reduce oxygen uptake which can ultimately lead to death
What might a pathologist expect to find in a body of a patient who died of suspected
TB?
Presence of TB bacteria
Enlarged lymph nodes
Tubercules (lesions) in lungs
Serious lung damage
Typical damage to brain, spleen, kidney, bones
Diagnosis of TB
Skin test (Heaf test and Mantoux test); uses protein tuberculin derived from dead bacteria;
detects whether body has anti-TB antibodies – inflammation reponse
Culture of TB bacteria from sputum
Prevention of TB
Treatment of TB
Use of specific antibiotics to kill the bacteria (a course can last more than 6 months and must be
completed to ensure all the bacteria are killed)
Antibiotics
Active TB bacteria are killed by using a combination of antibiotics
An antibiotic is a drug that kills or prevents the growth of bacteria.
Bacteriocidal
o Kill bacteria e.g. penicillins
Bacteriostatic
o Prevent the multiplication of bacteria
Antibiotics are used to kill or slow the reproduction of a pathogen to give the immune system the
chance to respond and ‘catch up’ so it can deal with the infection e.g. by phagocytes or antibody
production
Antibiotics target processes in bacterial cells but do not affect mammalian cells because:
they are eukaryotic
do not have cells walls
have larger ribosomes and subtle differences in the mechanism of protein synthesis
have different enzymes
Antibiotics do not affect viruses because antibiotics affect the metabolism of bacterial cells but
viruses have no metabolism so they cannot be affected.
Antibiotic resistance
Antibiotics are often over-prescribed or used when not really needed e.g. for colds, flu, other
viral infections
Patients stop taking them before the course in ended when they feel better but not all the
bacteria are killed)
Antibiotics used in low doses in diet of farm animals to make them grow faster so get passed
to humans in the food chain
The consequence is that the antibiotic is now ineffective so there is a need to:
use combinations of different antibiotics are used to reduce the probability of resistance to
both developing
only prescribe antibiotics when absolutely necessary**and complete the full course
of treatment
fight infections in other ways; infection control – use of disinfectants, hygiene (e.g.
hand washing and antiseptic or alcohol gels ); thorough cleaning of wards, clothing
(no ties, wrist watches!) **, use of gloves especially with open wounds
use of isolation wards **
improve diet, housing, living conditions so people more healthy so their immune systems are
better able to combat infections without the need for antibiotics
develop new antibiotics
develop other forms of treatment which do not involve antibiotics
HIV
HIV is found in blood and other body fluids; semen/vaginal secretions/breast milk
HIV infection occurs when blood or the body fluids containing the virus of an infected person gets
transferred directly into the body, and subsequently the blood, of an uninfected person by:
Unprotected sex
Direct blood to blood contact e.g.cuts, grazes, oral sex via gum damage/intravenous drug
abusers sharing needles
Mother to child across placenta, during birth or via breast feeding
Viruses reproduce by inserting their nucleic acid into the host cell which is then
translated into proteins to build new viruses.
Each DNA molecule (which makes up a chromosome) contains the genetic code for a large
number of proteins.
A gene is a region of a DNA molecule which codes for the synthesis of one particular
protein.
The genetic code of a gene is the sequence of bases in the DNA molecule that
codes for the order in which the amino acids are assembled into a polypeptide or
protein molecule (i.e. the primary structure).
It is a triplet code. A sequence of 3 bases codes for one amino acid (3 bases is the minimum
number to produce a code for the 20 amino acids)
A codon is the triplet of 3 bases coding for one amino acid
The code is non-overlapping: the codons are ‘read’ individually and in sequence (just like
reading the fat cat sat…) i.e. CTACTC is only read as two codons, CTA and CTC (rather than
CTA, TAC, ACT etc if the code was overlapping).
One codon codes for one amino acid only
The code is a degenerate code; there are actually 64 possible codons - most amino acids are
coded for by more than one codon, there is also one ‘start’ codon (AUG) and there are 3
codons which do not code for any amino acid and are called ‘stop’ codons.
The code is universal: the same triplet codes for the same amino acid in all organisms.
mRNA passes out of nucleus into cytoplasm and attaches to a ribosome on the RER
transfer RNA molecules carrying the amino acids specific to their anticodons pair up with their
complementary codons on the mRNA; the first one pairs up with the ‘start’ codon
to get the amino acids in the right place in the primary structure.
the amino acids are joined together by peptide bonds to form the protein.
process continues until the stop codon (for which there is no tRNA)
polypeptide released into the rER
the protein then folds to form its specific tertiary structure e.g. a viral capsid protein.
HIV Infection and AIDS
AIDS, acquired immune deficiency syndrome, is caused by infection with the human immunodeficiency virus, HIV.
HIV infection occurs when the body fluid (blood, vaginal secretions and semen, but not saliva
or urine) of an infected person is transferred directly into the body of an uninfected person.
This can occur This can occur when This can occur with This can occur from
through unprotected sharing needles, whether direct blood-to-blood mother to child across the
sex. used illegally or legally. transfer through cuts and placenta or in breast
grazes. milk.
HIV invades T helper cells and macrophages. The HIV gp120 molecules attach to their CD4 receptors allowing the virus
envelope to fuse with the host cell surface membrane, enabling the viral RNA to enter the cell.
Once inside, the virus uses reverse transcriptase to produce DNA from its RNA. The DNA is integrated into the host’s
DNA by another HIV enzyme, integrase. The viral DNA is transcribed and translated to produce new viral proteins and
assemble new viruses.
The new virus particles bud out of the T cell, taking some of the surface membrane with them as their envelope, and
killing the cell as they leave.
When a person is first infected by HIV, there is an acute phase of infection. There is rapid replication of the virus and loss
of T helper cells.
As the number of viruses increases, the number of host T helper cells decreases. Macrophages, B cells and T killer cells
are not activated and the infected person’s immune system becomes deficient.
The infected person may experience symptoms such as fever, sweats, headache, sore throat and swollen lymph nodes, or
they may have no symptoms.
The virus continues to reproduce rapidly, but the numbers are kept in check by the immune system.
T killer cells recognise the infected T helper cells and destroy them.
There may be no symptoms during this chronic phase, but there can be an increasing tendency to suffer various
infections which are slow to go away. Dormant diseases such as TB and shingles can reactivate. The chronic phase can
last for years, especially if combined with drug treatment.
An increased number of viruses in circulation (viral load) and a declining number of T helper cells indicate the onset
of AIDS, the disease phase.
The weakened immune system makes the patient more prone to opportunistic infections such as pneumonia and TB.
There may also be significant weight loss, dementia (memory and intellect loss) and the cancer Kaposi’s sarcoma.
AIDS is usually fatal.
Course of the disease
Acute phase
May suffer fever, sweats, headache, sore throat, swollen lymph nodes – similar to flu. (Some
people have no symptoms)
Lasts 3-12 weeks after infection
Rapid viral multiplication + loss of T helper cells.
Increase in HIV antibodies – now HIV positive
T killer cells destroy infected T helper cells, keeping numbers in check, so reducing rate of
viral multiplication, but numbers of helper T cells decreases as they are destroyed
Hopefully start to feel better!
Treating HIV
A number of new drugs are being designed to block fusion of HIV with its host cell to prevent
infection.
Inhibitors of reverse transcriptase, such as AZT, were the first anti-HIV medications, and are
still a critical part of treating infection.
Inhibitors of integrase are under study as a new way to block HIV replication
HIV protease inhibitors, one of the most potent types of anti-viral medications, block the
processing of other HIV proteins into their functional forms essential for virus maturation
before release
For this reason, based on our current knowledge, patients must remain on anti-viral therapy for
life. The drugs are very expensive and need to be taken for extensive periods of time so they are
not available to the vast majority of infected people
• Drug developers produce new drugs effective against pathogens (bacteria or viruses)
• These drugs provide a selection pressure;
• Rapid multiplication pathogens produces many with mutations
• Any pathogen with mutations that make them resistant to the drug will be more likely to
survive and reproduce; susceptible pathogens killed, resistant ones survive and increase
• Drugs now ineffective against resistant pathogens
• Drug developers have to create new drugs.