Topic 6 - Infection,

Immunity and Forensics

Sarah Newman
Time of Death
6.1

Understand how to determine the time of death of a mammal by examining the extent
of decomposition, stage of succession, forensic entomology, body temperature and
muscle contraction

As soon as a person dies, there is a series of physical and chemical changes that occur on and in the body. These
changes happen at different stages and as a result, we can pinpoint the time of death by examining the specific
stage which the body is at
 Extent of Decomposition
● After death, tissues start to break down and autolysis occurs which is when the body’s own enzymes break
down cells.
● Bacteria in the body then invade the tissues after death, releasing enzymes that result in decomposition.
The loss of oxygen in the tissues favours the growth of anaerobic bacteria
● Colour - First, putrefaction in humans is shown as a greenish discolouration of the skin in the lower
abdomen. This then spreads, darkens into a reddish-green colour before turning a purple black colour.
● Gas/liquid blisters may appear on skin due to production of gases like methane, carbon dioxide and
hydrogen sulphide that form in the gut. The body starts to smell, bloat and eventually starts to deflate as
gases are released
● When putrefaction fluid drains, soft tissue shrinks and rate of decomposition slows
● In a temperate climate, discolouration occurs between 36-72 hrs after death. Gas formation occurs after 7
days.
● Temperature of body determines rate of decomposition
● Low temperatures = slow decomposition rate, high temperatures = fast decomposition rate
● Rate of decomposition is highest between 21-38 degrees, intense heat obviously denatures enzymes
involved in autolysis, delaying start of decomposition.
Stage of Succession
● This overlaps with forensic entomology as corpses attract different types of insects, some that feed
on the body and others that feed on the insect.
● In this type of succession, one group of organisms feed on a decomposing body, conditions change
which attract another group of organisms. This series of stages continue until only the skeleton
remains
● Pioneer/colonising species are typically bacteria and blowflies.
● Secondary and beyond colonisers can be beetles, parasitic wasps.
● Species which are specific to colonising dead bodies can give you an accurate time of death
depending on its life cycle. The final species will be moths and beetles that will feed on dead bits of
skin and hair (keratin)
● Normally, eggs are laid in wounds or at openings of the body. Prevailing conditions determine the
community of species that first occupy the body and how this changes with each stage in the
succession. The season, weather conditions, size and location of the body all influence the number
and type of species present
 Forensic Entomology
The presence of insects allows a forensic entomologist to make an estimate of how much time has elapsed since
death. Forensic entomologists record information about the location and condition of the body by taking samples
of the insects and identifying the stage of their life cycle that organism is in.

● Occurs 48 hours and beyond, after time of death.

Variables:
● Temperature – if its cold, it will take insects longer to colonise - metabolism will be slower, there will be
fewer insects in cold conditions
● Clothing/coverings – stop entry of insects which slows the process
● Environment – number of insects available to colonise the body
● More entry points could lead to more insects (but not affect TOD estimate too much)
 Body Temperature
As soon as a person dies, their body temperature will decrease due to absence of exothermic chemical
reactions. The temperature of the body is useful for estimating time of death in the first 24 hours. When
alive, the internal temperature of the body is 37°, after death it will drop 0.50-2° per hour.

Core body temperature is measured through the rectum/abdominal stab. Environmental conditions must be
noted, as these affect how the body has cooled. The cooling of the body follows a sigmoid curve. Many
factors affect post mortem cooling like

● Body size - related to surface area and fat content

● Body position - related to surface area
● Clothing
● Air movement
● Humidity
● Surrounding temperature
Rigor Mortis (muscle contraction)
After death, muscles relax and then stiffen. This stiffening is known as rigor mortis. Joints become fixed in
position but after a while, rigor mortis passes and muscles are again relaxed. THe following events occur:

1. After death, muscle cells become starved of oxygen and oxygen dependent reactions stop
2. Cell respiration becomes anaerobic, producing lactic acid
3. pH of the cell falls, inhibiting the enzymes and thus inhibiting anaerobic respiration
4. The ATP needed for muscle contraction is no longer produced, as a result, bonds between the muscle
proteins become fixed.
5. Proteins can no longer move over one another to shorten the muscle, fixing the muscle and joints

Smaller muscles stiffen first before larger ones so complete rigor mortis takes between 6-9 hrs after death
Variables that affect rigor mortis are:
● Temperature – in the cold, rigor mortis is slowed down
● Exercise – if someone dies after a period of exercise then the majority of ATP will have been used up
and rigor mortis will set in quicker
● Drowning – if someone has died drowning then the struggle will have caused a lot of ATP to be used
up, same as above.
 Decomposition
6.2

Know the role of microorganisms in the decomposition of

organic matter and the recycling of carbon

Bacteria from the gut invade the tissues after death and
other bacteria and fungi from the surroundings colonise
the corpse, contributing to decay and changing
conditions on the decomposing body. These are
generally known as decomposers.

The organic carbohydrates, proteins, fats and nucleic acids found in corpses are great energy sources. This energy is
released through aerobic and anaerobic respiration in the form of carbon dioxide, and enables the bacteria/fungi to grow
and multiply rapidly, speeding up the process of decomposition. This recycles the carbon back into a form that can be used
in photosynthesis by plants, to synthesise organic molecules. Decomposition as a result, is a major process in sustaining the
carbon cycle
DNA Profiling
6.3

Know how DNA profiling is used for identification and determining genetic relationships between organisms (plants and
animals)

We use DNA profiling for:

● Screening for genetic conditions

● Studying evolutionary relationships
● Measuring genetic biodiversity
● Solving crimes – used within the FBI

A large amount of DNA doesn’t code for proteins and these non coding blocks are called introns (intragenic regions) and
are inherited in the same way as any genes within the coding regions; exons (expressed regions).

Within introns, short tandem repeats are found which are regions of noncoding DNA that contain sequences of repeated
bases. They occur at the same locus on both homologous chromosomes and the number of STRs vary for each individual
due to the fact that each person has a large number of introns with lots of STR loci.
DNA Profiling - the overall process
1. A tissue sample must be obtained and the DNA extracted
2. DNA is copied numerous times (amplified) by the polymerase chain reaction
3. Fragments are made by cutting the DNA at different lengths
4. Separation of fragments and visualisation through gel electrophoresis
5. Reference DNA profile is needed for comparison

The steps above are the basic stages that are required when undergoing DNA profiling.

1) Obtaining the DNA:

This DNA can come from animals and plants. Cells can be obtained through a cheek swab (saliva), blood, sperm or bone
marrow. DNA extraction:

● Tissue sample is broken down in a buffer solution that includes salt and detergent to disrupt the cell membranes
● The small suspended particles, including the DNA, are separated from the rest of the cell debris by filtering or
centrifuging
● Protease enzymes are incubated with the suspension to remove proteins and then cold ethanol is added to
precipitate out the DNA. Several stages of washing the DNA in buffer solution follows
More on DNA profiling
2) The Polymerase Chain Reaction

● This process uses DNA primers which are short DNA sequences complementary to the DNA next to the STR.
● The DNA primers are marked with a fluorescent tag
● The extracted DNA is placed in a tube (in a PCR machine) containing the DNA primers, nucleotides and DNA
polymerase.
● The tube undergoes a series of temperature changes. The first separates the double stranded DNA at 95 degrees,
the second optimises binding of primer to target DNA sequence at 55 degrees. The final temperature which is 70
degrees is the optimum temperature for the heat stable DNA polymerase to attach and nucleotides are added
which replicate the DNA.
● As the cycle continues, huge numbers of the DNA fragments are produced.
● In forensic cases, DNA samples are generally analysed for the presence of 10 STRs. Each target STR is four bases in
length and an additional primer is used to determine gender, targeting a sequence on the sex chromosome
3) Creating the Fragments

● Treat the DNA sample with restriction enzymes (restriction endonucleases). These enzymes are found naturally in
bacteria where their function is to cut up invading viral DNA.
● The enzymes cut DNA at specific base sequences
● If the restriction sites are either side of the STR then that fragment of DNA remains intact when it is separated from
the rest of the genome
● Bacterias own DNA isn't affected by their restriction enzymes as their DNA does not contain the sequences that are
targeted by their restriction enzymes.
● If the same restriction enzyme is used to cut two identical DNA samples, identical fragments are produced

4) Gel Electrophoresis

● Separated according to their size

● DNA is placed on a gel of agarose which provide a stable medium through which the fragments can move
● Gel is submerged in buffer solution and connected to electrodes, providing a potential difference
● Negatively charged DNA fragments migrate through the gel according to their overall charge and size. Smaller
fragments, with small numbers of repeat sequences travel faster and they end up closer to the positive electrode
● Over time, a DNA ladder is made and the fragments are measured in base pairs
4) Visualising the fragments

● As the gel is quite fragile, a nylon membrane is placed on top of the gel to give integrity.
● Dry absorbent paper is placed on top of the membrane which draws the buffer solution up through and carries the
DNA fragments so they are transferred onto the nylon membrane.
● The membrane is then incubated with an excess of a
labelled DNA probe and this probe binds to any
complementary sequences. This probe is usually
labelled with radioactive phosphorus.
● With a radiolabeled probe, the membrane is washed,
dried and placed next to x ray film and the film blackens
wherever the probe has bound with the DNA to form
double stranded fragments.
● A single band occurs on the profile where a person's
maternal and paternal chromosomes have the same
number of repeats at a particular locus. Two bands
occur on the profile if the two chromosomes have a
different number of repeats at a locus.
● A unique banding pattern for each person is created if
probes for many different repeated sequences are used.
 PCR
6.4

Know how DNA can be amplified using the polymerase chain reaction

As previously mentioned, the polymerase chain reaction aka PCR is used to amplify DNA so there is enough
to make a DNA profile. And it consists of a mixture containing the DNA sample, free nucleotides, primers,
DNA polymerase. The DNA polymerase is taq polymerase which has a higher specific temperature where it
can bind to the primers
This is essentially what happens:

At 95 degrees, the hydrogen bonds between the two DNA strands break (denaturation)
At 56.5 degrees, primers bond to the ends of the strands (annealing)
72.5 degrees is when the Taq polymerase binds to the primers and then uses complementary base pairing to
form a strand of DNA using the free nucleotides (elongation)
 Bacteria vs Viruses
6.5

Be able to compare the structure of bacteria and viruses

Bacteria:

● Bacteria are larger than viruses and are

considered living
● They do not have a nucleus or membrane bound
organelles and do not produce a spindle during
cell division
Bacteria vs Viruses
Viruses

● Smaller than bacteria and have a simpler structure. They

basically consist of a strand of nucleic acid (either DNA or
RNA) enclosed within a protein coat.
● They are non living as they can’t exist without a host cell as
they use the host’s metabolic systems to make more
viruses.
● The viruses genetic material is contained within a capsid
and instead of a cell wall they have a protein coat
● After reproducing inside the host cell, viruses either bud
from the cell surface or burst out of the cell, splitting it
open. When the cell splits, it dies and this is known as lysis.
The cells contents are released which can damage other
cells. These processes cause disease symptoms produced
by the virus.
● Some viruses have an outer envelope taken from the host cell's surface membrane; this envelope contains lipids
and proteins which help the virus attach to the cell and penetrate the surface membrane.
TB and HIV
6.6

Understand how Mycobacterium Tuberculosis (TB) and Human Immunodeficiency Virus (HIV) infect human
cells, causing a sequence of symptoms that may result in death
TB
• TB is caused by Mycobacterium tuberculosis and is the disease of the lungs and only 30% of people exposed to TB will
become infected and only 5-10% will develop symptoms.
Primary Infection
● Lasts several months with no symptoms
● Mt causes an inflammatory response from the host's
immune system. They travel to the lungs and attack
lung tissue as well as inhibit T lymphocytes through
suppression (reducing antibody production)
● Macrophages engulf the bacteria and a mass of scar
tissue known as a tubercule forms
● These tubercules are anaerobic and contain the
macrophages with dead/dormant Mt
● Bacteria evade the immune system by being taken up
within macrophages and surviving due to their
thick,waxy cell walls, making them difficult to
breakdown.
● The bacteria can lie dormant for years - latent TB and
slowly reproduce
● As a result the person shows no signs of the disease
but a weakened immune system can cause secondary
infection
Secondary Infection
● Also known as active tuberculosis. This is when the dormant
bacteria become active and start dividing. This could be because
the number of bacteria is too great, recurrent infection, age,
malnutrition, AIDS etc.
● With active tb, the bacteria multiply and destroy the lung tissue,
creating holes or cavities. The lung damage will eventually kill
the sufferer if not treated with an appropriate antibiotic.
● Symptoms include fever - worse at night (due to chemicals
released by neutrophils affecting the hypothalamus), coughing
caused by damage to lung tissue, sputum, weight loss and a
weakened immune system (as T lymphocytes are inhibited)
● Mt can also spread to bone marrow
● Mt mutates fairly rapidly, therefore evading the immune
response
More on TB

● Spread through inhalation of droplets

● Resistant to many types of antibiotic
● The fever enhances immune function and phagocytosis. It’s said that bacteria and viruses may
reproduce more slowly at the higher temperature.
● The lung damage will eventually kill the suffered due to insufficient oxygen absorption.
HIV
• HIV infection is caused by the Human Immunodeficiency Virus. HIV does not survive well outside of the body
and can only be transmitted through bodily fluids.
• HIV infects T-Helper cells which results in their destruction and therefore the weakening on the immune
system.
• The initial symptoms of HIV infection include fevers, tiredness and swollen glands. HIV antibodies may not
appear in the blood until 12 weeks after infection. During this stage, the T helper cell count falls rapidly.
• T killer cells begin to recognise and destroy infected T helper cells. This slows the replication rate of the virus
down.
• All symptoms may disappear for many years as the replication rate is controlled.
• Eventually, the T helper count falls to a critical value and the infected person is more likely to get opportunistic
infections such as TB. AIDS is the condition where the immune system deteriorates and fails
• HIV has gp120 molecules on its surface. These bind to the CD4 receptors on T helper cells. The virus envelope
fuses with the cell membrane and the viral RNA from HIV is released into the host cell. Reverse transcriptase
converts viral RNA in viral DNA. Integrase enzyme then inserts viral DNA into the host's DNA. New viral proteins
are now made through transcription and translation. The cell surface membrane of the host may be "stolen" to
form a new envelope
More on HIV
❖ Once the new viral proteins are made they bud out of the T cell and take some of the host cell membrane so
they can then infect new host cells. As they do this they kill the cell.
❖ When the T killer cells kill the T helper cells, the T helper cell count decreases which results in macrophages, B
cells and T killer cells not being successfully activated and therefore do not function properly.
❖ AIDS doesn’t always follow HIV directly. There are several stages - depends on factors:
● Health of host before infection
● Lifestyle
● Genetic resistance
● Quality of immune response
● Availability of drug treatment

HIV is split into three phases; the acute phase, the chronic phase and the disease phase
Acute Phase
● HIV antibodies appear in blood
after 3-12 weeks
● The infected person may
experience symptoms such as
fever, sweats, headache, sore
throat and swollen lymph nodes
or no symptoms
● There is rapid replication of the
virus and loss of T helper cells
● After a few weeks, infected T
helper cells are recognised by T
killer cells, which start to
destroy them. This reduces the
rate of virus replication, but
does not totally eliminate it
Chronic Phase
● Sometimes called the latent
phase
● Virus continues to reproduce
rapidly but the numbers are kept
in check by the immune system
● There may be no symptoms
during this phase, but there can
be an increasing tendency to
suffer colds or other infections,
which are slow to go away
● Dormant disease like TB and
shingles can reactivate
● Lasts for many years especially
combined with drug treatment
Disease Phase
● Eventually increased
number of viruses in
circulation and a declining
number of T helper cells
indicates the onset of AIDS,
the disease phase
● The decrease in the number
of T helper cells leaves the
immune system vulnerable
to other diseases. A normal
T helper cell count is over
500 per mm3. Below 200
per mm3, there is high risk
of infection by opportunistic
infections
 Non Specific Immunity
6.7: Understand the non specific responses of the body to infection, including inflammation, lysozyme action,
interferon and phagocytosis

Your body can get infections from pathogens entering the body, through broken skin, infected areas,
orifices or swallows
Inflammation
Your body will detect the foreign antigen on the pathogen and then the damaged cells cause an
inflammatory response. Histamines cause inflammation which increases the permeability of capillaries
to white blood cells (white blood cells produce histamines).
Inflammation also causes vasodilation - this increases blood flow to the area causing redness and
swelling and allows more white blood cells to arrive at the infected area

Lysozyme action
Lysosomes are membrane bound organelles which contain the enzyme lysozyme and they are found all
throughout your body but particularly at orifices. Lysozymes break down the chemical bonds in the cell wall of
bacteria causing their contents to leak out (lysis) and as a result, destroys the bacteria. Specifically the active
site on the lysozyme targets peptidoglycan in the bacterial cell wall
Non Specific Immunity
Interferon
Interferon are categorised as cytokines; a group of signalling proteins produced by the body’s cells as a defence
response to viruses. Interferon stimulates infected cells and those nearby to prevent the virus from replicating
from within them. Further virus production is therefore inhibited.
They also active the white blood cells (T helper cells) and promote inflammation

Phagocytosis
A phagocyte is a type of white blood cell that engulfs pathogens and destroys them using lysozymes. It is the
first line of defence to the general immune response.
1) The phagocyte identifies the foreign antigen
2) Phagocyte engulfs pathogen into phagocytic vacuole
3) Lysosomes fuse with phagocytic vacuole which release lysozymes
4) This hydrolyses the pathogen (breaking down cell wall)
5) The bacterial contents are released, killing the bacteria and those foreign antigens are then displayed on
the phagocyte surface, becoming an antigen presenting cell
Antigens and Antibodies
6.8: Understand the roles of antigens and antibodies in the body's immune response including the involvement of
plasma cells, macrophages and antigen presenting cells

Plasma Cells:
Plasma cells are differentiated clones of B effector cells which are part of the humoral response. They secrete lots of
the complementary antibodies which are specific to the pathogens antigen. These antibodies will bind to the antigens
on pathogens, forming antigen-antibody complexes.

The antibodies will help to clear infections three ways:

1) Agglutinating Pathogens - each antibody has two binding sites so an antibody can bind to two antigens at a
time, as a result, the pathogens become clumped together. Phagocytes will then bind to these antibodies and
phagocytose the pathogens all at once
2) Neutralising toxins - antibodies can bind to the toxins produced from pathogens which prevents them from
affecting human cells, so the toxins are neutralised and then phagocytosis occurs
3) Preventing the pathogen binding to human cells - when antibodies bind to the antigens, they block the cell
surface receptors needed to infect the host cells
Antigens and Antibodies
Macrophages
Macrophages are a type of white blood cell that are phagocytes. Phagocytes generally refer to cells
that are capable of engulfing cells but macrophages are white blood cells that do that.
Macrophages undergo phagocytosis and they can become antigen presenting cells.
Antigen Presenting Cell
Phagocytes are antigen presenting cells - they display the foreign antigens of the pathogen on their
cell surface in order to activate T cells. B cells also become an antigen presenting cell when it binds
to an antigen with a complementary receptor.
Protein fragments (peptides) from the pathogen become attached to proteins in the cell, these are
added to the macrophages cell surface membranes where they’re displayed as non self antigens.
 Antigens and Antibodies
We know what antigens are, but what are antibodies?

● Proteins with specific primary structure and specific

tertiary structure. Antibodies are complementary to
antigens
● They are made up of four polypeptide chains - two heavy
chains and two light chains. Each chain has a variable
region and a constant region
● The variable region - forms antigen binding site. Variable
regions differ between antibodies
● The hinge region allows flexibility when the antibody
binds to antigen
● Constant region allow binding to receptors on immune
system cells (same in all antibodies)
● Disulphide bridges hold the polypeptide chains together
 B cells and T cells
6.9: Understand the differences between the roles of B cells (B memory and B effector cells) and T cells (T helper, T killer and
T memory cells) in the body’s immune response.

T Cells

Activated by antigens presented by a phagocyte. The surface of T cells are covered with CD4 receptors that are a
complementary shape to the antigen (specific) and this activates the T cell. The T cell then divides (clones itself
through mitosis) and produces T helper cells, T killer cells and T memory cells.

T memory cells remain for months to years in the body so if the same pathogen (with same antigen) were to
invade the immune system, the response would be quicker. The T memory cells will kill the pathogens rather than
producing antibodies.

T killer cells are part of the cellular response and they destroy any cells with antigens on their surface membrane
that are recognised as foreign or nonself. This includes body cells infected with pathogens

T helper cells wil activate T killer cells and B cells

B cells and T cells
B cells

B cells are part of the humoral response and there are many types of B cell which are coated with antibodies.
These antibodies will be specific to a certain antigen which will be displayed by the T helper cells or the
pathogen.

The B cell will bind to a T helper cell and release cytokines which stimulate division (mitosis) and differentiation
of the B cells. The B cells will differentiate into either B effector cells or B memory cells.

B effector cells - these differentiate and divide to produce plasma cells which release antibodies into the blood
and lymph.

B memory cells - like T memory cells these are long lived cells that remain in the bond enabling an individual to
respond to the same pathogen with the same antigen in a much quicker response. During the secondary
immune response, B memory cells will activate, clone and produce plasma cells which will then produce plasma
cells
 Post Transcriptional Changes
6.10: Understand how one gene can give rise to more than one protein through post-transcriptional changes to
messenger RNA.

The DNA sequence of a gene contains introns and exons. Introns are sections of DNA that don’t code for amino
acids while exons are the coding sections of DNA.

Between transcription and translation, pre-mRNA is edited with the introns being removed through a process
called splicing. This takes place in the nucleus and is a post transcriptional change. After this splicing, mRNA will
now be formed and alternative splicing will remove some exons to form different mRNA strands

As a result, different mRNA strands can be formed from the same genes so we can say that more than one protein
can be produced from one gene. An example is antibodies, there are two types of antibody; secreted (free) and
membrane bound (attracted to surface of cells).
 Pathogenic Routes
6.11: Know the major routes that pathogens may take when entering the body and understand the role of barriers in
protecting the body from infection, including stomach acid, gut flora, skin flora and skin.

How do pathogens get in?

1) Cuts in the skin

2) Through digestive system (contaminated food)
3) Through respiratory system (inhalation)
4) Through other mucosal surfaces (nose, mouth and genitals)

Skin - a physical barrier to pathogens, blood clotting will seal the wound but before that process is complete,
pathogens can enter the bloodstream

Stomach Acid - contains hydrochloric acid with a pH that is less than 2, this aims to kill most bacteria that enter with
food. Some may survive though where they pass into the intestines, invade cells and cause disease
Pathogenic Routes

Gut flora and skin flora - the linings of your intestine and surface of your skin are covered in billions of
harmless microbes. They compete with the pathogens and thus limits the number of pathogens living in the
gut and on the skin. The gut flora specifically have a mutualistic relationship where bacteria aid the digestive
process and competitively exclude the pathogenic bacteria by secreting lactic acid

Mucous membranes - the secretion of mucus traps microbes and the beating cilia will carry mucus to the
mouth to be swallowed where the acidic conditions of the stomach kill it. Secretions in the mouth, nose and
eyes contain lysosomes which break down bacterial cell wall
 Immunity
6.12: Understand how individuals may develop immunity (natural, artificial, active, passive)
First of all, we need to discuss the primary and secondary immune response.

PRIMARY
● First immune response
● Slow, long time to recover
● T cells - B cells - plasma cells
● Symptoms expressed
● Specific antigen and antibody
saved in memory cells

SECONDARY
● Second immune response
● Fast, quick recovery
● Memory B cells - plasma cells - antibodies
● Memory T cells - kill pathogens
● No symptoms expressed
● Lots of antibodies produced
Immunity
ACTIVE IMMUNITY PASSIVE IMMUNITY

● When your immune system makes its own ● You get given antibodies which have already been
antibodies after being stimulated by an antigen. made. The immune system does not produce them
● There are two different types of passive immunity:
● There are two different types of active immunity:
1) Natural - antibodies are given by mother to child
1) Natural - primary response - produce antibodies - (through placenta and breast milk)
memory cells 2) Artificial - given antibodies via injection usually
2) Artificial - via vaccination of an attenuated ● Fast protection
pathogen to cause a primary response and make ● Doesn’t make memory cells so short term
antibodies
● Slow
● Long term
● Respond to antigen
The Evolutionary Race
6.13: Understand how the theory of an evolutionary race between pathogens and their hosts is supported by
the evasion mechanisms shown by pathogens

What is the evolutionary race?

Strong selection pressures exist for both host and pathogen. We are evolving to have more efficient immune
systems that fight a greater variety of pathogens in lots of different ways while pathogens have evolved
better ways to evade the immune systems. This competition between pathogen and host is known as the
evolutionary race. Sometimes, pathogens have the edge in this race because their reproductive cycle is
faster than ours and their population size is greater.

We can apply this theory to two examples, HIV and tuberculosis

The Evolutionary Race - HIV
● HIV has a high rate of mutation in the DNA of its antigen gene.
● This changes the tertiary structure of the HIV antigen causing antigenic variability
● Memory T cells don’t recognise the new antigen and so the secondary immune response is not
possible and the primary immune response will occur. The infected cells as a result are not killed

The Evolutionary Race - Tuberculosis

● The Mt bacteria infect the lungs and undergo phagocytosis. Here, they produce substances that
prevent the lysosome fusing with the phagocytic vacuole so the bacteria aren’t broken down and
they can multiply undetected inside phagocytes
● Antigenic variability also occurs so antigen presentation is disrupted and T cells, as a result, are
not activated
 Antibiotics
6.14: Understand the difference between bacteriostatic and bactericidal antibiotics

BACTERIOSTATIC BACTERICIDAL
● Prevent the multiplication of bacteria. ● Kills the bacteria
The host's immune system can then ● Reduces number
destroy the fewer number of bacteria ● Inhibition of bacterial cell wall synthesis which
● Inhibition of nucleic acid synthesis, leads to lysis
replication and transcription which ● Disruption of the cell membrane, causing
prevents cell division and synthesis of changes in permeability that lead to cell lysis
enzymes
● Inhibition of protein synthesis so
enzymes and other essential proteins
are not produced

Antibiotics do not work in viruses and they only target bacteria as they are prokaryotes so they have a
different cell wall with different ribosomes and antibiotics target these differences
Hospital Codes of Practice
6.15: Know how an understanding of the contributory causes of hospital acquired infections have led to codes
of practice regarding antibiotic prescription and hospital practice that relate to infection prevention and
control.
Antibiotic Resistance:
Hospital Acquired Infections:
● Using antibiotics creates a strong directional
selection pressure
● Infections caught in hospital
● Only most resistant organisms will survive and
● Many people are sick reproduce
● Some people are immunosuppressed ● Caused by overuse of antibiotics
● Transferred by coughing/sneezing etc ● Not finishing course of antibiotics
● Resistance can be transferred between bacteria
Prevention:
Prevention:
● Improve codes of conduct
● Don’t use antibiotics for minor/viral infections
● Clothing rules for staff
● Finish course of antibiotics
● High temperature laundry ● Use a range of narrow spectrum antibiotics wherever
● Handwashing for staff and visitors possible