BIOLOGY UNIT 4

THE NATURAL ENVIRONMENT

AND SPECIES SURVIVAL
Topic 6 Infection, immunity and
forensics

Investigating time of death

Temperature of a body can give some
indication of how long a person has been
dead.
The presence of absence of rigor mortis
also can be used to estimate time of death.
The stage of succession of organisms on a
corpse combined with information on the
species life cycles in similar conditions and
temperatures can help to estimate time of
death (known as forensic entomology).

Transcription
The process which forms mRNA.
Double helix is unzipped as hydrogen bonds
between bases are broken by RNA polymerase.
The prime DNA strand (template strand) is used to
order the sequence of nucleotides in an RNA
transcript. RNA polymerase joins many small
nucleotide units together to form mRNA.
Every triplet code of DNA gives rise to a
complementary codon on the mRNA. Every
thymine is replaced with uracil.
mRNA passes through the pores in the nuclear
membrane where they then move to the surface
of the ribosomes.

Translation
tRNA is found in the cytoplasm, and consists of a
unit of three bases known as the anticodon and
an amino acid.
Ribosomal RNA holds together the mRNA, tRNA
and the enzymes controlling protein synthesis.
Each mRNA strand has a start codon (AUG) and
a stop codon (UAA, UAC or UGA). The mRNA
becomes attached to a ribosome and the
ribosome starts reading it and coding for the
complementary amino acid.
Then, tRNA lines up its anticodon alongside the
complementary codon in the mRNA. Hydrogen
bonds form between bases, peptide bonds join

Post-transcriptional changes
In recent years, it appears to have been shown that
the one gene, one polypeptide theory is over
simplistic.
The RNA transcribed from DNA is now called premRNA and contains some nonsense sections that
do not code for any protein, known as introns.
The areas of the RNA that do code for the
polypeptide chains are known as exons.
Before the mRNA lines up on ribosomes after
transcription, the ends are capped so that it is not
attacked by enzymes, the introns are removed, and
the exons are joined together in a process called
RNA splicing. This is carried out by enzymes
known as spliceosomes.

DNA profiling
Individuals and species can be identified through
patterns in their DNA. Introns are the regions
used in DNA profiling.
There are short sequences of DNA within introns
that are repeated many times. Mini-satellites
have 20-50 bases repeated from 50 to several
hundred times. Micro-satellites have 2-4 bases
repeated 5-15 times.
DNA strands are chopped into fragments using
restriction enzymes (e.g. restriction
endonucleases), which cut the DNA molecule at
specific base sequences known as recognition
sites.
The fragments are separated using gel

DNA profiling
Gel contains a dye that binds to the DNA
fragments. The dye will fluoresce when placed
under UV light, so the known DNA can be
compared with the unknown DNA to identify it
following completion.
An electric current is passed through the
apparatus and the DNA fragments move at
different rates towards the positive anode
(due to negatively charged phosphate groups).
The next stage is Southern blotting. An alkaline
buffer solution is added to the gel and a nylon
filter placed over it. Dry absorbent paper is used
to draw the solution containing the DNA to the
filter, which then blots onto it. The alkaline

Polymerase chain reaction (PCR)

PCR is used to amplify the DNA to allow for DNA
profiling to take place by adapting the natural
process in which DNA is replicated in the cell.
The DNA sample to be amplified, along with
DNA polymerase, primers and a good supply of
the four nucleotide bases are mixed together
in a PCR vial and placed in a PCR machine where
they are heated to 90-95C. This causes the
DNA strands to separate as the hydrogen bonds
break, and when the mixture is then cooled to 5560C the primers can bind to the single DNA
strands.
It is then reheated to 75C where polymerase
works to build the complementary strands

Viruses
Smallest of all the microorganisms
They are arrangements of genetic material and
protein that invade other living cells and take over
their biochemistry to reproduce
They contain DNA or RNA with either double or
single stranded nucleic acid
Viral DNA acts directly as a template for both new
viral DNA and for the mRNAs needed to synthesise
viral protein
Viral RNA uses the enzyme reverse transcriptase
to produce DNA molecules corresponding to the
viral genome, which acts as a template for new viral
proteins
They have protein coats made up of capsomeres

Viruses
There is
considerable
variation in
the
structure of
viruses, but
they all
contain a
few key
features.

Virus life cycles

1. Bacteriophage attacks bacterium and attaches to it
2. Viral (phage) DNA is injected into host cell, bringing
about synthesis of viral enzymes
3a. Viral DNA incorporated into host cell DNA. Viral DNA
replicated
each time the bacterium divides. (lysogenic pathway)
OR 3b. Phage DNA inactivates the host DNA and takes
over cell chemistry. (lytic pathway).
4. Phage DNA is replicated. New phage particles are
assembled and protein coats form around the viral DNA.
Lysozyme is synthesised or released.
5. Lysis bacterial cell burst due to action of lysozyme,
releasing up to 1000 new phages to infect more bacteria.
[Some types of virus have both the lysogenic and lytic
pathway in their life cycle, but others move straight to the
lytic stage after infecting a cell. During the period of lysogeny,

Virus life cycles

Retrovirus life cycle

Retroviruses (e.g. HIV) contain viral RNA, and so
cannot be used as mRNA but must be translated
into DNA by the enzyme reverse transcriptase
in the cell cytoplasm.
This viral DNA then passes into the nucleus of
the host cell where it is inserted into the host
DNA. This is then transcribed by transcriptase
enzymes to make viral mRNA and new viral
genome RNA.
New viral material is synthesized, and leaves the
cell via exocytosis, taking some of the host cell
membrane and eventually killing the cell through

Bacteria structure
*= not present in all bacteria

Bacteria structure
Capsule protects the bacterium from phagocytosis by white
blood cells. Also covers the cell markers on the cell
membrane which identify the cell, making it easier for
bacterium to be pathogenic.
Flagella helps to move the bacterium by rapid rotations.
Some plasmids also code for particular aspects such as the
production of a toxin or resistance to an antibiotic.
Bacterial cells walls have a peptidoglycan layer, made up
of many parallel polysaccharide chains with peptide crosslinkages.
Gram staining can be used to identify Gram-positive
bacteria (thick peptidoglycan layer, turns teichoic acid
purple/blue) and Gram-negative bacteria (thinner
peptidoglycan layer, has no teichoic acid so turns red).

How bacteria reproduce

Most commonly, bacteria reproduce through asexual
reproduction by splitting in two (binary fission). Once
a bacterium reaches a certain size, the genetic material
replicates into two identical sections and the cell splits.
However, there are rare forms of other reproduction
that sometimes take place:
Transformation a short piece of DNA is released by a
doner and actively taken up by a recipient cell.
Transduction a small amount of DNA is transferred
from one bacterium to another by a bacteriophage.
Conjugation genetic information is transferred by
direct contact.

How are pathogens transmitted?

Vectors A living organisms transmits infection from
one host to another. Many insects are vectors. (e.g.
malaria)
Fomites inanimate objects that carry pathogens, such
as hospital towels and bedding. (e.g. Staphylococcus)
Direct contact direct contact spreads many skin
diseases. (e.g. gonorrhoea)
Inhalation coughing and sneezing release droplets
which can spread infections if inhaled. (e.g. influenza)
Ingestion passed through contaminated food or drink.
(e.g. salmonella)
Inoculation directly through break in the skin. (e.g.
HIV)

Barriers to entry
Skin toughened by keratin to prevent penetration.
Produces sebum that inhibits the growth of
microorganisms.
Mucus (e.g. in respiratory system) traps
microorganisms. Contains lysozymes, enzymes which
rupture bacteria by disrupting their cell walls.
Lysozymes are also present tears, milk and saliva.
Blood clotting prevents entry of further pathogens
when skin breaks.
Saliva and earwax bactericidal properties, kills
bacteria.
Hydrochloric acid in stomach destroys ingested
microorganisms.

Non-specific immune response

The non-specific response simply recognises the difference
between self and non-self and reacts against anything
foreign.
Inflammation mast cells and damaged white blood cells
release chemicals called histamines, triggering vasodilation
causing local heat and redness. The raised temperature
reduces pathogen effectiveness. The histamines also make
the capillary walls leaky, so plasma, white blood cells and
antibodies are forced out of the capillaries causing swelling
(oedema), and these can then destroy the pathogen.
Fever the hypothalamus resets to a higher body
temperature, which reduces the pathogens ability to
reproduce and allows the specific immune response to work
more effectively.

Non-specific: Phagocytosis
Phagocyte describes white blood cells which engulf and
digest pathogens. There are two main types: neutrophils
and macrophages. They accumulate at site of infection to
attack.
A phagocyte recognises the antigens on a pathogen.
The cytoplasm of the phagocyte moves round the
pathogen, engulfing it.
The pathogen is now contained in a phagocytic vacuole
in the cytoplasm of the phagocyte.
A lysosome fuses with the phagocytic vacuole. The
lysosomal enzymes break down the pathogen
The phagocyte then presents the pathogens antigens.
It sticks the antigens on its surface to activate other
immune system cells

Specific immune response

There are two main types of lymphocytes
involved in the immune system; B cells, made in
the bone marrow and mature in the lymph
glands, and T cells, made in the bone marrow
but mature in the thymus gland.
T cells are mainly T killer and T helper cells. T
killer cells produce chemicals that destroy
pathogens. T helper cells are involved in
producing antibodies.
The process of these cells working is reliant on
special proteins known as MHC proteins, which
display antigens on the cell surface membrane.

Specific: The humoral response

Consists of the T helper activation stage and the
effector stage.
In the T helper activation stage, following
phagocytosis, the macrophage presents the
pathogenic antigen as an MHC protein complex on
the cell surface and becomes known as an antigenpresenting cell (APC).
CD4 receptors on the membrane of T helper cells
enable it to bind to the specific antigen on the MHC
complex. This triggers T helper cells to produce
clones; most become active T helper cells, but
some become T memory cells which remain in the
body and rapidly become active if the same antigen
is encountered a second time.

Specific: The humoral response

During the effector stage, B cells and T cells are active.
B cells engulf pathogens and can also present the
antigens on MHS complexes, becoming another type
of APC.
A T helper cell from the active clone recognizes the
specific antigen on the B cell and binds to it, triggering
the release of cytokines from the T helper cell which
stimulate the B cell to form clones. These can be B
effector cells (which then differentiate into plasma cell
clones to produce antibodies) or B memory cells.
Antibodies work in a variety of ways. They can reduce
the ability of pathogens to invade host cells, help prevent
them spreading, and the antigen-antibody complexes
may stimulate other reactions to destroy the antigen.

Specific: The cell-mediated

response
When the pathogen is inside a host cell (e.g. virus),
the humoral response is not very effective, so the
cell-mediated response is used.
The pathogen is digested and antigens presented on
MHC complexes on an APC.
T killer cells bind to the antigen/MHC complex. If
exposed to cytokines from an active T helper cell,
this then triggers the production of clone T killer
cells and T killer memory cells.
T killer cells release enzymes which perforate the
membrane of infected cells, making them swell
with water and burst (induced apoptosis). Any
pathogens released are labelled with antibodies and
destroyed.

Antibiotics
Work by the principle of selective toxicity
they interfere with the metabolism or function of
the pathogen with little damage to the human
host.
Antimicrobial action

Example
antibiotic

Antimetabolites interrupt metabolic

pathways, e.g. blocking nucleic acid
synthesis

Sulphonamides

Prevent formation of cross-liking in cell

walls so bacteria burst

Beta-lactams, e.g.
penicillin

Damage the cell membrane so

metabolites leak out/water leaks in

Some penicillins

Protein synthesis inhibitors prevent

successful transcription/translation so
protein is affected

Tetracyclines

Antibiotics
Bacteriostatic inhibits the growth of the
microorganism.
Bacteriocidal will destroy almost all of the
pathogen present.
Broad spectrum antibiotics target a wide range
of harmful bacteria, pathogens, and neutral and
good bacteria.
Narrow spectrum antibiotics target one or two
specific pathogens.
Effectiveness depends on concentration of drug
in affected area of body, local pH, susceptibility of
pathogen, dosage etc.

Infection prevention and control

There are several ways to prevent infection,
particularly in hospital settings where healthcareacquired infections are problematic:
Controlling the use of antibiotics (prevents
resistant bacteria)
Hygiene measures (prevents spreading through
contact)
Isolation of patients (when infected, to prevent
spread of infection)
Prevention of infection coming into the hospital
Monitoring levels of healthcare-acquired
infections

Different types of immunity

Natural active immunity e.g. coming into
contact with foreign antigen. Your own body
produces the antibodies.
Natural passive immunity e.g. breastfeeding.
Antibodies received through mothers milk.
Artificial passive immunity e.g. injection
containing antibodies to prevent development of
a disease, but does not give prolonged immunity.
Artificial active immunity e.g.
immunisation/vaccination. Own body produces
antibodies, but source is artificial.

Tuberculosis
Spread by droplet infection, drinking infected milk or
working in close contact with cattle
Active TB symptoms fever, night sweats, loss of
appetite, loss of weight, tiredness, coughing (blood).
If immune system is healthy upon infection, a mass
of tissue called a tubercule will form containing the
bacteria. After about 8 weeks the immune system
controls the bacteria and inflammation dies down.
Some tuberculosis can avoid the immune system, so
may survive. The bacteria produce waxy layers
which protect from enzymes, and can lie dormant
for years until the person is weakened, and may then
produce active tuberculosis.

HIV/AIDS
HIV attaches to the CD4 receptors on T helper
cells and infects them. It is a retrovirus, so takes
over the host DNA and replicates (see previous
slide on retrovirus replication). When it leaves the
host T helper cell, it is destroyed.
At the same time, the host T killer cells recognise
and destroy some of the heavily infected T helper
cells. The result is a great reduction in the
number of T helper cells, which means that the
activation of many macrophages and T killer cells
does not take place, so immunity is lowered and
the individual is vulnerable to secondary infections.
(progresses to AIDS)

HIV/AIDS