Immunity, Infection & Forensics
Immunity, Infection & Forensics
Immunity, Infection & Forensics
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Forensics and Time of Death
Time of death of a mammal can be determined by looking at the following:
• Extent of decomposition – bodies usually follow the same pattern of decay and
decomposition, and therefore a stage of decomposition can be used to determine
how long a body has been dead for.
• Stage of succession - as the body decays, the species colonising the body change.
Therefore, analysis of the community of species present can be used to determine
time of death.
• Forensic entomology – each species of insects has a specific life cycle. Determining
the age of insects present enables the time of death to be determined.
• Degree of muscle contraction – after death muscles begin to stiffen. This is called
rigor mortis, and the extent of rigor mortis can be used to determine time of death.
However, the stiffness only lasts around 36 hours, so is only useful to an extent in
determining time of death.
Microorganisms such as bacteria and fungi play an important role in the decomposition of
organic matter and the recycling of carbon. Bacteria and fungi secrete enzymes that
decompose dead organic matter into small molecules which they then use as respiratory
substrates – carbon dioxide and methane are released in this process, thus recycling
carbon.
DNA Profiling
DNA profiling is a forensic technique used for identification and determining genetic
relationships between organisms:
1. Fragments of DNA are cut with restriction endonuclease enzymes (either side of
satellites).
2. These fragments are separated and visualised using gel electrophoresis - fragments are
placed in wells in agarose gels and dyed with ethidium bromide so they fluoresce under
UV light. A current is then applied to the gel. DNA is negative but fragments of different
sizes move differently according to mass so ‘bands’ appear.
3. Southern Blot - alkaline buffer solution added, nylon filter - dry absorbent material
draws solution containing DNA fragments to the filter - fragments visible as ‘blots’.
Gene probes (complementary sequences labeled with genes like fluoresce or
radioactivity) are added and bind with DNA (hybridisation).
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4. ‘Blots’ compared and number of satellites visualised as a graph (repeated sequences of
DNA in introns are referred to as mini/microsatellites depending on their size. The
more closely related two people/species are, the more similar the repeats are).
Before the sample can be analysed via DNA profiling, the sample needs to be amplified
using Polymerase Chain Reaction:
1. A reaction mixture is set up by mixing the DNA sample, primers, free nucleotides and
DNA polymerase which is the enzyme involved in creating new DNA strands.
2. The mixture is then heated to 95 degrees to break the hydrogen bonds and to separate
the two strands.
3. The mixture is then cooled to a temperature between 50-65 degrees depending on the
type of primers used, so that they can bind to the strands.
• Bacteria are prokaryotic cells, meaning that they do not have a nucleus – their
genetic material is stored in the form of a circular strand of DNA. Viruses consist of
just nucleic acid (DNA or RNA) enclosed in a protein coat.
• Bacteria do not require a host to survive, whereas viruses are entirely dependent on
their hosts and cannot survive without them.
• Bacteria have a cell membrane, cell wall and cytoplasm, as well as other organelles
such as ribosomes, plasmids, flagellum and pili. Viruses possess no such structures.
An example of a bacterial disease is tuberculosis (TB). TB is caused by a bacteria called
Mycobacterium tuberculosis which infects phagocytes in the lungs:
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• First infection is symptomless. Infected phagocytes are sealed in tubercles as a result
of an inflammatory response in the lungs.
• Bacteria lie dormant inside the tubercles. They are not destroyed by the immune
system, as tubercles are covered with a thick waxy coat.
• When the immune system becomes weakened, the bacteria become active again,
and slowly destroy the lung tissue, thus leading to breathing problems, coughing,
and weight loss, as well as fever.
• TB can be fatal.
• After several weeks HIV antibodies appear in blood, thus making a person HIV
positive.
• After this period, the symptoms disappear until the immune system becomes
weakened again, thus leading to AIDS.
Response to Infection
• Gut and skin flora – natural bacterial flora competes with pathogens for food and
space.
Non-specific responses of the body to infection include:
• Fever – the hypothalamus sets body temperature higher. This decreases speed of
pathogen reproduction and increases rate of specific immune response.
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• Phagocytosis is a process in which white blood cells engulf pathogens thus
destroying them by fusing a pathogen such as bacteria enclosed in a phagocytic
vacuole with a lysosome.
The specific immune response is antigen-specific and produces responses specific to one
type of pathogen only. This type of immune response relies on lymphocytes produced in
the bone marrow:
• B cells mature in the bone marrow and are involved in the humoral response.
• T cells move from the bone marrow to the thymus gland where they mature, they
are involved in cell-mediated response.
1. The host cell displays the antigens on its Major Histocompatibility Complexes and
becomes an Antigen-Presenting Cell.
3. Cytokines secreted by active T Helper cell stimulates the T Killer cell to divide by mitosis.
4. T Killer cell divides to form active T Killer cells and T Memory cells.
5. Active T Killer cells bind to APCs and secrete chemicals which cause pores to form in the
cell membrane.
Humoral Response
T Helper Activation:
4. The T Helper cell is ‘activated’ and divides by mitosis to form T memory cells and
active T helper cells.
Effector Stage:
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1. Antigens from APCs that are complementary to the antibodies on B cells bind and
are taken in by endocytosis.
3. An activated T helper cell (from the previous stage) with a complementary receptor
protein to the antigens binds to the APC. It produces cytokines.
4. Cytokines stimulate the B cell to divide by mitosis and form B memory cells and B
effector cells.
7. Effects of antibodies:
Immunity
Immunity can either be active or passive; active immunity results from the production of
antibodies by the immune system in response to the presence of an antigen whereas
passive immunity results from the introduction of antibodies from another person or
animal.
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• The secondary infection has less lag (so less time for symptoms), is more rapid and
produces more antibodies and T Killer cells than the primary response because there
are Memory T and B lymphocytes in circulation from the primary infection.
1. Gene is transcribed which results in pre-MRNA (the transcript of the whole gene).
2. All introns (non-coding regions) and some exons (coding regions) are removed.
3. The remaining genes are joined back up by enzyme complexes called spliceosomes. The
same exons can be joined in a variety of ways to produce several different versions of
mature functional RNA.
Antibiotics
Antibiotics can also be used to fight infection by killing the bacteria and stopping their
growth. There are two types of antibiotics:
• Bactericidal antibiotics kill bacteria by destroying their cell wall, thus causing them
to burst.
• New patients are screened at arrival, isolated and treated if they are infected to
prevent the spread of bacteria between patients.
• Antibiotics are only used when needed and their course is completed to ensure
that all the bacteria are destroyed, and to minimise the selection pressure on
bacteria, to prevent resistant strains from forming.
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• All staff must follow the code of practice which includes strict hygiene regimes such
as washing hands with alcohol based antibacterial gels and wearing suitable
clothing which minimises the transmission of resistant bacteria.
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