MODULE 7

INQUIRY QUESTION 1: HOW ARE DISEASES TRANSMITTED?

DISEASE: A condition of living organisms or one of its parts that impairs normal functioning and is typically
manifested by distinguishing signs and symptoms.

Signs: objectively measurable factors (e.g. Body temp, rash etc. )

Symptoms: factors reported by patient that can not be directly observed by others (e.g. fatigue)

INFECTIOUS DISEASE: caused by an infectious agent (pathogen), and are often communicable.

PATHOGEN: organisms or biogenic molecules that can cause diseases. They are infectious agents, meaning they
can be transmitted between individuals.

PATHOGENICITY: The ability ( # of pathogens needed) to cause disease.

7.1.1 DESCRIBE A VARIETY OF INFECTIOUS DISEASES CAUSED BY PATHOGENS,

INCLUDING MICROORGANISMS, MACROORGANISMS AND NON -CELLULAR PATHOGENS,
AND COLLECT PRIMARY AND SECONDARY -SOURC ED DATA AND INFORMATION
RELATING TO DISEASE TRANSMISSION

CLASSIFYING DIFFERENT PATHOGENS THAT CAUSE DISEASE IN PLANTS AND ANIMALS

Macroorganism: can be seen and is living

Microorganism: cannot be ween with naked

eye and is living.

Non-cellular Pathogen: non-living.

Endo: inside, Ecto: outside

Type Description Examples

Prion Abnormal protein (causes degeneration of CNS and fatal). Kuru, CJP
Do not contain any genetic material and are smallest of
all pathogens.

Disease causing prions have a different structure to

normal prion proteins found within brain and spinal
chords. Pathogenic prions induce abnormal folding
patterns in normal proteins that they contact. The
abnormal proteins are then deposited within CNS and
other organs.

Virus Contains a capsid protein coat that contains genetic Influenza, COVID-19, Mumps
material (nucleic acids) non-living. Can only reproduce via
a host cell. (Once a virus attaches to a cell, it enters and
takes over the cell’s reproductive systems, replicating
itself. Once the host cell becomes full, it bursts and the
new virus repeat the process). 25-50nm in size

Bacteria Single celled, prokaryotic, reproduces by binary fission. Whooping cough, T.B, tetanus
Cell wall made of cellulose. Replication time: 10min – 24
hrs

Protozoan Microscopic, single-celled eukaryote 1-300 micrometres malaria

in size.

Fungi Eukaryotic cell wall made of chitin. Saprophytic – live on Ringworm, tinea (athletes foot), oral
dead tissue. Unicellular or multicellular thrush

Macro- Endoparasites: live inside host body Ectoparasites: live Pin worm, tick
parasites outside body use blood for nutrients and some can inject
toxins.
INVESTIGATING THE TRANSMISSION OF A DISEASE DURING AN EPIDEMIC

Points of entry/exit:

o Skin
o Pathogen can spread through blood
o Respiratory: mouth, nose, throat and lungs
o Pathogen may lead to mucus and can exit via coughing and sneezing.
o Gastrointestinal: includes stomach, large intestines, mouth and rectum as entry points
o Pathogen can cause vomiting and diarrhoea.
o Genitourinary: reproductive and urinary systems with pathogens exiting via urethra or vagina.

DESIGN AND CONDUCT A PRACTICAL INVESTIGATION RELATING TO THE MICROBIAL

TESTING OF WATER OR FOOD SAMPLES

AIM: to design and conduct a practical investigation relating to the testing of food and water samples

Independent variables: the type of food/water sources

Dependant variable: the amount and type(species) of microbial growth

Controlled variables:

o Using a sterilisation loop and heating in a hot flame for the same duration of time
o Not touching any part of the sterilisation loop post flame exposure thus no microbes present from
other sources
o Keeping agar plates the same size and exact concentration of nutrients
o Keep the agar lid on until time to gently swab the agar jelly with the sterilisation loo from the intended
food swab

[What would impact independent variables]

THE CONTROL: a sealed agr plate not exposed to any of the food/water sources( independent variable)

RISK ASSESSMENT:
 Risk hazard prevention

The flame from Burning skin causing skin Wearing appropriate PPE, keeping the burner on
Bunsen Bruner irritation and injury yellow flame unless necessary to allow the flame to
be visible. Keep all long hair tied up

Agar plate, Potential exposure to disease- Keep lid and seal on the agar plate after removing it
microbial causing microbes, and pathogens from the incubator. Wear gloves and wash hands
growth from agar source with water when handling agar plate

MATERIALS:

o Sterilisation loop
o Matches
o Bunsen burner
o Sticky tape (seal)
o Food sources: strawberries blue vein cheese, honey, natural Greek yoghurt
o Water sources: tap water, bottled water, dam water

METHOD:

1. Appropriate PPE ( safety glasses, apron and surgical gloves) are worn.
2. The sterilisation loop was placed into a Bunsen burner flame and moved back and force for a minimum
of 10 seconds
3. The selected food source was gently swabbed with the sterilised loop three times
4. The lid was removed from the agar plate and the loop containing swabbed food source was gently
transferred onto the surface ( creating an inoculated plate as seen in the diagram)
5. The lid was placed black on and sealed tightly with tape
6. The loop was sterilised again as in step 2
7. Repeat steps 1-6 for all food and water types
8. Place inoculated agar plates into an incubator for 24 hours at 35ºC
9. Post 24 hours, the inoculated agar plates were viewed with lid and seal intact
10. The microbial types (species) and the amount were identified and recorded

Results:

Interpreting agar plates (FEMSOC): Form, elevation, margin, surface, opacity, colour.
 o Bacterial colonies: White/cream, circular/irregular, small, defined margin, look wet and shiny.
o Fungal colonies: Appear fuzzy, filamentous margin, powder-like.
o Yeasts: White, glossy.
o Mould: White/grey/green, fuzzy.

INVESTIGATE MODES OF TRANSMISSION OF INFECTIOUS DISEASES, INCLUDING DIRECT

CONTACT, INDIRECT CONTACT AND VECTOR TRANSMISSION

o Pathogens must either travel by direct contact, indirect contact or vector transmission.
o If a disease can be transmitted easily, it is considered virulent.

DIRECT TRANSMISSION INDIRECT TRANSMISSION

Occurs when host directly contacts the non- o Airborne transmission

infected organism, such as through: o Touching infected surface
o Contamination of food and water
o Touching
o Infected surgical equipment
o Sexual contact
o Blood contact e.g. measles, flu.
o Biting

e.g. HIV, herpes, skin infections (chickenpox)

TRANSMISSION VIA VECTORS

Vectors are living immediate organisms that carry pathogens unknowingly. It is a specific type of indirect
transmission and generally involves anthropoids ( like mosquitoes) with blood-sucking.

e.g. malaria (vector: mosquitos and pathogen protozoan) , heartworm.

Reservoirs: non-living objects that hold pathogens, act as breeding spot for them. E.g. soil or water

Formites: lifeless objects that acts as a carrier of infection to transfer infection from infected individual to
unaffected. E.g. doorknobs.

7.1.2 INVESTIGATE THE WORK OF ROBERT KOCH AND LOUIS PASTEUR, TO EXPLAIN THE
CAUSES AND TRANSMISSION OF INFECTIOUS DISE ASES

KOCH’S POSTULATES
Proved that diseases were caused by microscopic agents (pathogens). He injected the anthrax bacteria bacillus
into healthy sheep, which developed anthrax, to prove a micro-organism grown outside of body could cause
disease.

HIS POSTULATES:

1. The microorganisms must be found in abundance in all

organisms suffering from the disease, but not found in
healthy organisms.
2. The microorganism must be isolated from diseased
organisms and grown in pure culture.
3. The cultured organism should cause disease when
introduced to healthy organisms.
4. The microorganism must be reisolated from the
inoculated, diseased experimental host and identified
as being identical to the specific causative agent.

Note: only applicable to living organisms, i.e. does not apply to

viruses.

PASTEUR’S EXPERIMENTS ON MICROBIAL CONTAMINATION

o Discovered most diseases are caused by micro-organisms.

O Assisted wine makers by describing micro-organisms that cause fermentation and explained that these
microbes can be killed by heating the wine, known as pasteurisation.
O He demonstrated that infectious agents cause disease, and discovered how to make vaccines from
weakened agents. E.g vaccine against cholera in chicken.
O Invented process of pasteurisation (killing microbes through heat)
AIM: to conduct experiments similar to Louis Pasteur’s swan neck flask to disprove spontaneous generation.

HYPOTHESIS: The exposed broth with a straight neck will display

microbial growth.

METHOD:

1. Place the broth equally between 4 flasks and boil for 5

minutes
2. Top 2 flasks with a curved glass tube and the other flasks
with a straight glass tube
3. Allow to sit in a shaded area for 2 weeks and observe for
signs of contamination- cloudiness, colour change, colony
growth.

Observations

Curved Tube No noticeable change after 2 weeks

Straight Tube Significant discolouration, Fungal colonies on both surfaces, Broth cloudy, Up to 4
different colonies on one surface

Discredited theory of spontaneous generation. His method led to the development of pasteurisation to avoid
microbial contamination of food and drinks by killing microbes.

7.1.3 ASSESS THE CAUSES AND EFFECTS OF DISEASES ON AGRICULTURAL PRODUCTION,

INCLUDING BUT NOT LIMITED TO:

PLANT DISEASES

Diseases in plants can lead to:

- Death of plant
- Necrosis (tissue destruction).
- Abnormal growth
- Reduced yields of grains, pastures, fruits and vegetables.
- Loss of trading opportunities nationally and internationally.
- Economic loss for farmer.
- Dire consequences on Australian economy as it relies heavily on exports of grains, fruits and vegetables
Example: Potato blight:

o When potatoes were imported into Ireland, they reproduced asexually, producing genetic copies.
o When a potato was infected by the fungal pathogen phytophthora, the entire crop was destroyed since
every potato was susceptible to disease.
o Host: potato Pathogen: phytophthora.
o Symptoms: rotting of leaves
o Environmental factors: humid soil, no genetic diversity
o Host factors: they were in close proximity = easy transfer.

ANIMAL DISEASES

Diseases in farm animals can lead to :

o Death of animals
o Economic loss to farmers
o Loss of appetite and weight of animals

Example: Foot rot in sheep:

o Host: sheep, Pathogen: bacteria, dichelobacter nodosus.

o Symptoms: painful abscesses between toes → lameness and weight loss due to inability to graze.
o Environmental factors: pathogen need dense, wet, humid and warmer environment, survives in
soil for max 4 days.
o Host factors: sheep with dry intact tissue remained non-infected, dermatitis must be present for
bacteria to form infection, overgrown hooves create reservoirs for bacteria.
o Not exotic disease as not introduced from different area.

7.1.4 COMPARE THE ADAPTATIONS OF DIFFERENT PATHOGENS THAT FACILITATE THEIR

ENTRY INTO AND TRANSMISSION BETWEEN HOSTS
 Adaptions to facilitate adhesion/invasion Transmission route
o Mainly unknown.
o Piggyback other proteins to facilitate movement through the gut. o Vertical(mother to child)- can
o Secrete substances that allow invasion of lymphoid tissues. transmit across placenta.
o Prions then invade nervous tissues and travel to brain. o Indirectly through infected
meat.,
Prions

o Direct contact (can be blood-

Adhesion: borne, using red blood cells to
facilitate growth).
o Viral surface proteins adhere to surface of host cell. o Indirect contact with fomites.
o Airborne transmission- can
Invasion:
stimulate sneezing and can
o Virtues enter cell through endocytosis (viruses are enveloped and remain suspended in air
enclosed in membrane) or by delivering viral genome through pores in
membrane.
Viruses

o Direct contact
Adhesion: o Indirect contact (fomites)
o Airborne- stimulate sneezing,
o Use pili and fimbria (hair like structures on their surface) resist drying out in air.
o Adhesins on surface resist washing action of urine, mucus, cilia. o Vector-borne transmission –
o Form a biofilm (community of bacteria attached to a host surface.) produces proteins to attach to
vectors
Invasion:

o Enzymes break down cell.

o Capsule of biofilm resist phagocytosis.
Bacteria

o Chemicals destroy immune defences.

o Toxins are secreted to damage cells.
o Use pili and
o Faeco-oral (infected food and
protozoan

o Microtubule penetrates host cell and facilitates entry, membrane is water) induces diarrhoea and
formed to protect from lysosomes. transmission.
o Direct contact

o Direct contact
Adhesion: o Airborne transmission
o Soil-borne – form endospores to
o Assisted by cell wall/capsule molecules. resist drying (desiccation),
stable in range of conditions.
Invasion:

o Thermotolerance – heat shock proteins cope with body temperatures.

o Cell wall and capsules protect fungi from host attacks.
Fungi

o Secretion of hydrolytic enzymes damages host cells and provides

nutrients.
micropara

Hookworms: : Secrete proteins that reduce host cell responses. o Direct contact.
sites

Ticks :Secrete molecules t prevent vasoconstriction, clotting or inflammatory

response.
INQUIRY QUESTION 2: HOW DOES A PLANT OR ANIMAL RESPOND TO INFECTION?

7.2.1 INVESTIGATE THE RESPONSE OF A NAMED AUSTRALIAN PLANT TO A NAMED

PATHOGEN THROUGH PRACTICAL AND SECONDARY INVESTIGATION

PLANT RESPONSE TO PATHOGENS

Plants have passive (physical and chemical barriers) and active( once the pathogen is recognised) defences
against defences.

Passive defences:

Physical barriers:

o Including thick cuticle, cell walls and small stomata, preventing pathogen entry
o Plants with thicker cuticles are better defended from pathogens that can secrete enzymes to break
down the cuticle.
o Bark offers plants extra protection.
o Vertical hanging leaves, which do not accumulate water film, reduce the chance of pathogen reservoirs
building.
o Stomata open during rain to regulate water balance, but can be a entrance for pathogens.

Chemical barriers:

o Chemical compounds within plant tissue can limit fungal and bacteria growth.
o Plants can produce enzymes to break down pathogen-derived toxins.

Active response?????

FUNGAL PATHOGENS
 Australian Native plant (host) Pathogen fungus

Common name Crimson Bottlebrush Myrtle rust - disease name

Scientific name Callistemon citrinus Puccina psidii

Description/characterist o grow to around 1.5-4m but can reach 9m o Fungal pathogen, part of a specialized group of
ics o Cylindrical, brush like flower spikes fungi called “rust fungi.” These fungi are
o Drooping branches obligate parasites, i.e. they can only grow on
o Tiny creamy white nubs close to stem living host.
o Bright red stamens o Requires darkness, moisture, and temperatures
o Fruiting capsules along stem of 15-25º to germinate.
o Dark green hairy leaves with mint scent

Diagram of
organism/agent

How does pathogen Rust spores travel kilometres through natural and
invade (adaptations of biological agents. These spores germinate and the myrtle
pathogen and action it rust fungus grows, piercing plant cells to obtain nutrients
from the plant. The growth of new pustules on the plant
takes)
can mature and release spores in 10-12 days. These
spores remain viable for 3 months.

Detailed outline of how As the rust attacks young, soft and actively growing
the plant responds to leaves, the bottlebrush leaves produce chlorotic
pathogen’s invasion spots on the underside. Around 14 days later, these
spots can be found on the upper leaf surface. These
lesions then turn brown and grey, producing masses
of yellow spores. Severe rust disease can kill shoot
tips. Warm sunny days with morning dew provide the
perfect condition for myrtle rust infections. Some
plants may struggle to reproduce, or compete with
other species that are more susceptible to disease.
Easily spread via wind, human acitivty and animals.

signs/symptoms of that Deformed leaves, leavy defoliation of branches, -

the plant shows stunted growth and often plant death.

VIRAL PATHOGENS
7.2.2 ANALYSE RESPONSES TO THE PRESENCE OF PATHOGENS BY ASSESSING THE
PHYSICAL AND CHEMICAL CHANGES THAT OCCUR IN THE HOST ANIMALS CELLS AND
TISSUES

Any foreign material is flagged by the body, since the surface of the “agent” does not have the same markers as
one’s own body. The surface ,markers stimulate an immune response and are called antigens. Pathogens are
recognised by the antigens they have on their surface.

INQUIRY QUESTION 3: HOW DOES THE HUMAN IMMUNE SYSTEM RESPOND TO

EXPOSURE TO A PATHOGEN?

7.3.1 INVESTIGATE AND MODEL THE INNATE AND ADAPTIVE IMMUNE SYSTEMS IN THE
HUMAN BODY

INNATE IMMUNITY SYSTEM:

Innate immunity: provides a first and second line of defence against pathogens. It is genetically programmed (at
birth) and is non-specific.

1ST LINE OF DEFENCE

Consists of physical and chemical barriers to pathogens:

CHEMICAL:

o SEBUM AND SWEAT: oily and microbial properties, purpose is to waterproof and lubricate skin.
o Acne-bacteria and ear infections
o LACRIMAL SECRETIONS: tears wash away pathogens and contain enzymes to break down unwanted
matter.
o Conjunctivitis, Trachoma
o ACIDIC SECRETION: gastric acid lower pH
o Herpes, Gonorrhoea
o LYSOSOMES: digestive enzymes to breakdown and destroy virus
o Common cold, Measles
o URINE: sterile until lower urethra. Acidic, antimicrobial peptides secreted by lining of urinary tract to
prevent binding of bacteria to epithelial cells.
o GASTRIC STOMACH SECRETIONS: stomach wall secretes hydrochloride acid which creates very
acidic environment, discouraging growth and survival of microbes.
o SALIVA: mixture of water, mucus, electrolytes and enzymes, that has a flushing action against microbes
due to the antimicrobial properties.

PHYSICAL

o SKIN: a dry seal, waterproof and a barrier for internal tissues, preventing pathogens from entering.
o Leprosy, ringworm
o CILIA: tiny microscopic hairs that beat up within mucosa lining to move foreign particles and pathogens
towards the outside
o Urinary tract and Sinus infection
o PERISTALSIS: automatic muscular movement along the oesophagus keeps mucus and particles,
potential microbes, moving through the body. Lack of movement can cause bacterial growth.
o Esophagitis
o COAGULATION of blood to reseal any wounds if skin is broken
o MUCOUS MEMBRANE: moist, pink tissues lining digestive, respiratory and genitourinary systems,
allowing substances to enter if necessary but will trap pathogens, removing them by sneezing or
coughing.
o SPHINCTERS: circular muscle that maintains constriction of natural body passage
o TIGHT JUNCTIONS: between endothelial cells lining red blood cells that form a physical barrier
between extra cellular tissues and blood stream.
o URINE: flushing and cleaning urethra frequently to prevent and remove microbial growth
 o VOMITING AND DIARRHOEA: reflex action by the brain. Method of expelling harmful substances or
pathogens in the gastrointestinal system.
o Mucus: moist and sticky which traps pathogens so that pathogens don’t enter the body through the
trachea and into the lungs.
o E.g. cholera and food poisoning.

2ND LINE OF DEFENCE

o initiated by chemical signalling from damaged tissue and consists of the inflammatory response and
phagocytosis by WBCs.
o Nonspecific
o Occurs when pathogen passes through barriers of 1st line.
o Non-specific response (innate) to immediately fight off any pathogens before they cause damage in the
body.

INFLAMMATION

o An area of inflammation will turn:

o red (increased blood flow),
o hot( increase in temp due to micro circulation )
o swollen(to isolate pathogen and make environment unfavourable),
o pain due to chemical mediators of inflammation
o When infected, cells will release chemicals (histamines) to activate this response. Chemicals that
increase temperature are also released to inhibit pathogen growth and survival.
o These chemicals increase vasodilation to allow white blood cells ( neutrophils, macrophages and
dendritic cells) to enter site of infection by fitting through blood vessel cells.

PHAGOCYTOSIS : process of engulfing

 o Carried out by phagocytes, a specialised white blood cell that engulfs pathogens.
o They then attack and destroy pathogens.
o Neutrophils:
o First on the scene and quick acting, self-destruct after engulfing pathogens if not useful
o Useful for acute (short term) infections
o Macrophages:
o Longer lasting, used in fighting chronic (longer) infections.
o Engulfs and destroys pathogens then display antigens of infection on its surface for 3rd line of
defence.
o Along with dendritic cells, act as bridges between innate and adaptive immune system.
o Cell death: when body cannot fight infection, granulomas can be formed which are produced by host
to encapsulate pathogen and seal it
o It is a capsule of dead cells, trapping infected cells inside, killing those cells and any pathogens
too.
o E.g. leprosy and T.B

FEVER :

o Pyrogens (fever-causing chemicals) are released by phagocytes into the blood where they travel to the
brain, causing body temperatures to rise to 40° to inhibit pathogen growth and survival. Can also
enhance activity of white blood cells strengthening response to pathogen.

If both fail, pathogens gain access to the body and enter the bloodstream and are transported around the body.

ADAPTIVE IMMUNITY (RESPONDS SPECIFICALLY TO PATHOGEN)

THIRD LINE OF DEFENCE

This line of defence is the reason vaccines work. The fist and second were non-specific, responding to any
foreign particles entering the body.

The third line is a very specific line, adaptive to each pathogen it fights, in turn remembering each pathogen it
fights to be prepared for any future infections.

1. The humoral response (antibody-mediated) is effective against pathogens in bodily fluids (humors).
2. The cytotoxic response (cell-mediated) is effective against intracellular pathogens.
a. Cells of the adaptive immune system have immunological memories , ‘remembering
pathogens.”
b. The adaptive immune system consists mostly of lymphocytes, killer T cells, helper T cells, B
lymphocytes and antibodies.
Innate Adaptive

Slow/delayed (3-5 days from primary exposure-first time exposed to

Immediate response
pathogen). 72-96hrs to generate antibodies

Builds memory- antigen-specific due to memory B and T cells. B

No memory
memory cells make plasma cells that make antibodies

Encoded in our genome Generated by an exposure

Present at birth Acquired throughout life

Receptors recognise general ‘non-

Receptors are antigen-specific (specific pathogens)
self’ markers

o Once the pathogen enters the host, the body is able to determine the pathogen to be foreign due to
the ANTIGEN.
o When a cell is infected, chemical indicators (interferons, chemokines, MHC-I &II) are released and
different WBC (lymphocytes) are created to fight specific pathogens. 2 major categories:
o T lymphocytes
o B- lymphocytes

B-LYMPHOCYTES

o Develop in Bone marrow, mature in lymph nodes and circulate in blood → extracellular
o Responsible for adaptive immune response outside cells
o Involved in the humoral response- occurs in blood and tissue fluids

PRIMARY IMMUNE RESPONSE

o B-cells identify pathogen when antibodies on its surface bind to a specific foreign antigen.
o B cells then become activated with the help of Helper T cells which release cytokines.
o The B cells then makes many copies of itself. These cells differentiate into 2 different types:
o Plasma B cells: produces antibodies ( also called immunoglobulin) against the pathogen.
o Memory B cells: remain in body for long periods of time, provide immunity for subsequent
infections.

SECONDARY IMMUNE RESPONSE

 o When the adaptive immune system is exposed to the same pathogen on subsequent occasions, there
is a more rapid response and a greater production of antibodies.
o This is why booster vaccines are recommended for various diseases.

ANTIBODIES

o Not all antibodies produced are the same or found in equal concentrations.
o Are Y shaped protein molecules that consist of 4 chains of protein – 2 larger heavy chains and 2 smaller
lighter chains.
o An antibody molecule has 2 binding sites, each site is specific for a particular antigen. Pathogens have
different epitopes (the region of an antigen molecule) on their surface that will bind to different
antibodies.
o When bound, the resulting molecule is called the antigen-antibody complex.

Images

o There are five different types of heavy chains which give 5 different antibodies: IgA, IgE, IgD, igG, IgM.
o Different classes act in different ways to neutralise a pathogen. The 5 ways are:
1. NEUTRALISATION: antibodies bind to and coat pathogens, blocking their activity.
2. AGGLUTINATION: neutralised pathogens clump together and are surrounded by antibodies.
3. PRECIPITATION of dissolved antigens.
4. ACTIVATION of the complement system, leading to cell lysis.
5. OPSONISATIOn: enhanced phagocytosis by natural killer cells (NK)

Images

T CELLS

o Develop in bone marrow, mature in the Thymus (T). More concentrated in the spleen, tonsils and other
parts of the lymphatic system. (intracellular)
o Killer (Cytotoxic) cells: recognise body cells infected with pathogen or damaged cells, releases
chemicals and causes infected cell to die.
o Helper T cells: stimulated by antigen-presenting cells. Interreact with other immune cells and produce
chemicals to stimulate phagocytes, B cells and cytotoxic T cells.
o Memory T cells: Remain in the body after a primary exposure to an antigen to allow a more effective
secondary response should re-exposure to same antigen occur.
o Regulatory T cells: immunosuppressors that help inhibit immune cells at the end of an immune
response.

CELL MEDIATED RESPONSE:

 o Responsible for elimination of pathogens inside host cells.
o Regulated by T cells (lymphocytes), mediated by the T cell receptors (TCR).
o T cells recognise fragments of/partially digested antigens only.
o T cells make direct contact wit infected cells via TCR.
o Receptor binding triggers signal transduction in the T lymphocyte, resulting in proliferation, cytokine
release and activation of cytotoxic function.
o Healthy cells have major Histocompatibility complex (MHC1) protein on their surface. When cells are
infected or when they are cancerous, they don’t produce that protein. MHCII is found in antigen-
presenting cells ( healthy MHC1 on surface) such as macrophages, dendritic cells and activated B cells.

PROCESS OF CELL MEDIATED IMMUNITY:

1. Foreign material engulfed by macrophages, displays antigens attached to their MHCII molecules.
2. Antigen-presenting macrophages move to lymph nodes, they are inspected by helper T cells that have
the T cell receptor that corresponds to the antigen being presented.
3. Helper T cells activate cloning of cytotoxic T cells and memory T cells that are specific for this antigen.
4. Cytotoxic cell leaves lymph nodes and migrate to site of infection. Antigen receptors in cytotoxic cell
bond with antigen on infected cells.
5. T cells then release chemicals that destroy the cell and any pathogens within it.
6. These chemicals also increase inflammation and attract more macrophages, which carry out
phagocytosis.
7. Some cytotoxic T cell produce a chemical called interferon, which protects the healthy cells around an
infected cell from viral invasion.
8. Once infection defeated, suppressor T cells (supress immune system) release other chemicals to stop
production and action of cytotoxic T cells.
9. Memory T cells specific to that particular antigen remain in the body (lymph nodes). On re-exposure to
the same antigen-containing pathogen, they cause rapid production if more of the same cytotoxic cells.
This prevents the body from developing symptoms of the disease again.

7.3.2 EXPLAIN HOW THE IMMUNE SYSTEM RESPONDS AFTER PRIMARY EXPOSURE TO A
PATHOGEN, INCLUDING INNATE AND ACQUIRED IMMUNITY

PRIMARY EXPOSURE : this is when the body first experiences a pathogen. The primary immune response creates

cytotoxic T-cells and plasma B-cells (producing antibodies). The production of antibodies is slow and low in
numbers.

o After being infected once by the pathogen (the primary exposure), you are left with a multitude of
memory T and B lymphocytes.
SECONDARY EXPOSURE:

o During the second exposure, the memory cells are able to detect the pathogen early and the response
by the immune system is far more effective.
o During the subsequential exposure, the production of antibodies is much quicker and far greater in
numbers. This response kills any pathogens, well before the pathogen can take hold and begin to
harm/damage the host (i.e. before any symptoms occur).

Add graph

VACCINES

o Humans use vaccines to help create an artificial experience of the primary exposure.
o A vaccine can introduce the body to a weakened/dead/enucleated version of the pathogen
9recognised by antigen) one that the body can easily fight off.
o Once the body has overcome the vaccine, the memory cells remain in the body to more effectively
fight off future infections.

TYPES OF VACCINES:

1. Live attenuated vaccines are alive but weakened pathogens. They’re most like a natural infection and
provide strong disease immunity. E.g. measles, mumps, chicken pox.
2. Inactive vaccines are inactive or killed pathogens. You may need several doses or booster shots over
time. E.g. hep A, flu and Pollio.
3. Toxoid vaccines protect against harmful substances 9toxins) produced by pathogen. They use
weakened versions of the toxins called toxoids. Booster shots may be required to maintain protection
against diseases. E.g. diphtheria and tetanus parts of the DTaP vaccine.
4. Subunit and conjugate vaccines use only a specific part of the pathogen. They provide strong immunity
to the key part of the germ. These vaccines may also require booster shots. E.g. The Hepatitis B
vaccine,
5. mRNA vaccines contain a special type of RNA called mRNA instead of using germs or toxins. mRNA
instructs cells to make the germ’s antigen, which triggers an immune response. These vaccines do not
carry live virus and do not change DNA. E.g. covid, Pfizer and Moderna.
6. Viral vector machines may use DNA ir mRNA to instruct cells to make germ’s antigen. The genetic
material is wrapped in a different safe virus to take instructions into cell. It does not exchange DNA.
E.g. covid-19 Astra Xeneca vaccine).

COMPLEMENT SYSTEM

o Group of 20 soluble proteins that assist other defence mechanisms in destroying extra cellular
pathogens.
 o These complement proteins can stimulate phagocytes to become more active, attract them to the site
of infection or destroy membranes of pathogen.
o The complement system is a part of the immune system that enhances (complements) the ability of
antibodies and phagocytic cells to trigger the following immune functions:
1. Membrane Attack – by rupturing cell wall of bacteria (classical complement pathway)
2. Phagocytosis - By opsonising antigens. C3b has most important opsonising activity.
(alternate complement pathway).
3. Inflammation – by attracting macrophages and neutrophils (lectin pathway).

o It is part of the innate immune response which is not adaptable and does not change during an
individuals lifetime.
o The complement system, however, can be recruited and brought into action by antibodies generated
by the adaptive immune system.

CYTOKINES

o A large and diverse group of proteins produced by a wide range of immune cells including
macrophages, neutrophils, B cells and T cells. they act as chemical messengers in both the innate and
acquired immune system.
o Roles include
o Attracting other phagocytes to an area of infection.
o Stimulating activity of NK cells.
o Inhibiting activity of all WBCs when infection is defeated.
o One group, interferons, interfere with the reproduction of viruses.
o Signalling cells to undergo apoptosis

MAJOR HISTOCOMPATIBILITY COMPLEX MOLECULES (MHC)

There are two classes of MHC molecules involved in adaptive immunity, MHC I and MHC II.
 o MHCI molecules are found on all nucleated cells ( contain nucleus); they present normal self-antigens
as well as abnormal or non-self pathogens to the effector T cells involved in cellular immunity.
o MHC II molecules are only found on macrophages, dendritic cells, and B cells; they present abnormal of
non-self pathogen antigens for the initial activation of T cells.

MHCI

o MHCI molecules found on all normal, healthy nucleated cells, signal to the immune system that the cell
is a normal ‘self” cell.
o In a healthy cell, proteins normally found in the cytoplasm are degraded by proteasomes (enzyme
complexes responsible for degradation and processing of proteins) and processed into self-antigen
epitopes; these self-antigen epitopes bind within the MHCI antigen-binding cleft and are then
presented on the cell surface.
o Immune cells such as NK cells, recognise these self-antigens and do not target the cell for destruction.
However, if a cell becomes infected with an intracellular pathogen (e.g. a virus), protein antigens
specific to the pathogen are processed in the proteasomes and bind with the MHCI molecules for
presentation of the cell surface.
o This presentation of pathogen-specific antigens with the MHCI signals that the infected cell must be
targeted for destruction along with the pathogen.

INQUIRY QUESTION 4: HOW CAN THE SPREAD OF INFECTIOUS DISEASES BE

CONTROLLED?

o Infectious diseases spread quickly among populations leading to pandemic events.

o New diseases are likely to become epidemic or pandemics, with most new diseases originating in
animals.
o

7.4.2 INVESTIGATE PROCEDURES THAT CAN BE EMPLOYED TO PREVENT THE SPREAD OF

DISEASE

HYGIENE PRACTICES

o Hygiene practices are effective in slowing rate of spread of contagious diseases while also preventing
them.

PERSONAL HYGIENE:

o Washing of hands or use of disinfectants to eliminate pathogens.

 o Covering mouth/nose when sneezing to prevent airborne transmission.
o Direct contact with items such as napkins should not be shared.
o Fruits and vegetables should be cleaned, and raw meat should be cooked properly.
o Garbage should be disposed off safely.

COMMUNITY HYGIENE:

o Garbage and sewage disposal

o Sterilisation of equipment in hospitals, dentists, salons.
o City planning to reduce overcrowding.
o Strict guidelines for commercial food handling, storage and serving.

QUARANTINE

o Quarantine practices limit the spread of pathogens by isolated infected hosts (whole organisms, live or
dead or products from animals/plants/people) until pathogen is eliminated, thus preventing
transmission form host to host.
o In Australia, the department of agriculture and water resource (DAWR) is responsible for maintaining
Australia’s reputation as a relatively disease-free country → exports valued.
o Quarantine laws prevent the entry of items that are deemed risky and thus prevent spread of diseases
from certain regions to another.

VACCINATION, INCLUDING PASSIVE AND ACTIVE IMMUNITY

Vaccination: inoculating an individual with an antigen, pathogen.

Immunisation: process of body building immunity for particular vaccine and thus pathogen.

o To gain acquired immunity and prepare host for any future challenge from the pathogen.
o Each vaccine is specific (3rd line of defence) for one type of antigen and will give immunity for only one
type of disease.
o Vaccines are vital to infectious disease control.
o Herd immunity can be achieved by vaccinating most of the population protect vulnerable individuals
such as elderly.

Active Acquired Immunity: Vaccination causes immune response to produce specific memory cells for antigen.

Passive acquired immunity: Involves introduction of specific antibodies for means of preventing a disease .
Developing immunity only lasts months as no memory cells are created by body.
PUBLIC HEALTH CAMPAIGNS

Raising awareness through education amongst the population and implementing public health programs can
control or prevent disease such as:

o Government regulations ensuring standardised procedures are followed. E.g. food handling,
sterilisation of equipment.
o Reporting of notifiable diseases allows strategies to be put in place.
o Public immunisation programs such as childhood immunisation to:
o Diphtheria
o Tetanus
o Whooping cough
o measles
o Population based health programs can be conducted such as:
o Screening of diseases
o Maternal and child health programmes.
o Include family planning as overpopulation is also responsible for certain outbreaks due to unhygienic
environment and close proximity.

USE OF PESTICIDES

Pesticides are designed to kill pathogens directly or eliminate the vectors that transmit them. E.g. DDT used to
kill insects that transmit disease.

However, there are problems associated with pesticides such as the ability of vectors and other pathogens to
build resistance, thus reducing effectiveness of pesticide and require development of stronger pesticides. This is
an issue as pesticides can have damaging effects on the environment.

GENETIC ENGINEERING

o Involves the altering of the genetic composition of organisms making them resistant to certain
diseases.
o E.g. transgenic species
o Not universally accepted:
o Concerns regarding the effects on the environment and biodiversity.
o Ethical issues to be considered.

7.4.3 INVESTIGATE AND ASSESS THE EFFECTIVENESS OF PHARMACEUTICALS AS

TREATMENT STRATEGIES FOR THE CONTROL OF INFECTIOUS DISEASE
ANTIVIRALS

Antivirals are used to treat a variety of viral diseases. Most antivirals are virus specific but some are broad-
spectrum ( they can treat many viruses).

Antivirals work on viruses by blocking their action at various points during infection, blocking the:

o Entry of virus into cell

o Reverse transcription of viral RNA into DNA
o Translation of viral DNA into proteins.
o Integration of viral DNA into the genome of the cell.

Effectiveness:

o Antivirals cannot cure the disease but reduce duration against the virus, reducing symptoms.
o Viruses most commonly targeted by antiviral drugs include: HIV, influenza A, Herpes and Hep B and C.
o As a preventative measure, they can decrease likelihood of sickness by 55%. They can also reduce
possibilities of developing severe illness and reduce chances of virus turning lethal for specific patient.
o However, it has a growing problem of resistance due to mutations.

ANTIBIOTICS

Antibiotics are widely used to treat diseases caused by bacteria.

o Antibiotics work by blocking vital processes in bacteria, killing the bacteria or preventing them from
replicating by preventing cell wall, nucleic acid or protein synthesis. This allows the body ‘s natural
immune system to fight the bacterial infection.
o Doctor’s prescribe antibiotics according to the bacteria that uses that specific infection. Occasionally
tests are done to identify bacteria and its sensitivity to antibiotics.

EFFECTIVENESS:

o Antibiotics are used in surgical procedures to avoid infections.

o Most antibiotics target the pathogenic bacterial cells rather than human cells and thus have minimal
side effects.

ANTIBIOTIC RESISTANCE:

o Occurs when bacteria change or mutate and become less sensitive to antibiotics.
o Misuse or overuse of antibiotics results in the likelihood of bacteria surviving, growing and multiplying
increases.
 o Mutated bacteria can also pass their genetic material to other bacteria, thus forming a strain of
antibiotic resistant bacteria.

REDUCING ANTIBIOTIC RESISTANCE:

o Taking antibiotics only for bacterial infections.

o Take antibiotics only as directed by doctor. Not following instructions may lead bacteria becoming
resistant.
o Taking the right antibiotic. Different infections require different antibiotics.

Similarities Difference
Antibiotic Both can be broad spectrum Treat bacterial infections
Both fight infection Large amount of resistance
antiviral Both reduce spread of disease They don’t kill, only inhibit growth
of virus.

7.4.4 INVESTIGATE AND EVALUATE ENVIRONMENTAL MANAGEMENT AND QUARANTINE

METHODS USED TO CONTROL AN EPIDEMIC OR PANDEMIC

And 7.4.1 :

7.4.1 INVESTIGATE AND ANALYSE THE WIDE RANGE OF INTERRELATED FACTORS

INVOLVED IN LIMITING LOCAL, REGIONAL AND GLOBAL SPREAD OF A NAMED
INFECTIOUS DISEASE

o Managing the environment during an epidemic reduces the pool of available pathogens.
o Environmental factors influencing spread or control of infectious disease: water supply, air quality,
sanitation facilities and food sources.
o Quarantine measures are designed to reduce the possibility of transmission of pathogens from infected
to non-infected hosts.
o E.g. good control seen in Ebola pandemic

Ebola epidemic:

Ebola is a severe infectious disease caused by the virus Ebola.

o Extremely contagious and causes rapid death.

o Transmitted via direct contact with bodily fluids and mucous membranes from infected individuals,
including sexual transmission.
o Also transmitted through animals that are reservoirs , e.g. fruit bats
 o Also burial rituals and direct contact of body of infected person.
o Incubation period: 2 – 21 days
o Symptoms: fever, fatigue, headache, progressing to vomiting, diarrhoea, bloody stools.
o (bleeding due to coagulation fever resulting from liver damage).
o Death rate for 1976 Africa outbreak was 50%.
o Management of disease: oral fluids to replace losses and maintain circulating blood volume,
medication for fever and pain.

Control of pandemic:

Environmental:

o Provision of facilities for barrier nursing (providing care in infection controlled settings)
o Water and hygiene controls
o Hand hygiene
o Safe waste management (ventilation control, sterilisation of equipment)
o Maintenance of personal protective equipment.

Quarantine procedures:

o Isolating patients in single rooms, or leaving 3m between beds.

o Same clinical staff and equipment assigned to each patient.
o Visits were restricted except for parents of child.
o Disposal of all sharp equipment in a puncture proof container.
o Surfaces were sanitised and cleaned daily.
o Any exposed people were people were isolated and monitored for 21 days.
o Border checkpoints were established with armed guards to manage movement in and out of
quarantine areas.

Longer term measures:

o Reducing animal-human transmission by ensuring meat is cooked properly.

o Wearing gloves when dealing with animal reservoirs
o reducing human-human transmission through:
o Hygiene
o Practicing safe sex for 12 months after infection.
o Prompt burial of the deceased

Local controls:

o Quarantine measures
o Prompt burial of the deceased
 o Social distancing
o Working with community leaders in poor communities to build collective trust and use of medical
practices.

Regional:

o Sterilisation of hospital and medical equipment

o Appropriate hygiene and equipment when handing animals
o Sourcing meat reliably

Global:

o Quarantine measures for people travelling from ebola affected contries

o Border control
o Declaration of symptoms.

7.4.5 INTERPRET DATA RELATING TO THE INCIDENCE AND PREVALENCE OF INFECTIOUS

DISEASE IN POPULATIONS, FOR EXAMPLE:

INCIDENCE: the number of new cases occurring during a specified time (infection rate).

PREVALENCE: the proportion of the population that have the disease at particular point in time 9refers to all

cases). Prevalence = no. of cases in period / population. * 100

MOBILITY : humans act as carriers for pathogens and may spread the disease to new locations when they move.

Refers to immigration and emigration patterns between regions, determining the ability of the pathogen to
spread easily.

e.g. ebola, mobility of population allowed for pathogen to spread across Africa quickly.

RATES OF IMMUNISATION : immunisation reduces disease transmission through a community. Percentage of

population that is immunised against an infectious disease, determining what percentage of po[pulation is
vulnerable.

Herd immunity: When a significant proportion if the population is immunised, this creates herd immunity as
lowers risk for unvaccinated from coming into contact with disease. Essentially all of population is immunised.
E.g. measles

MOBILITY OF INDIVIDUALS AND THE PORTION THAT ARE IMMUNE OR IMMUNISED

MALARIA OR DENGUE FEVER IN SOUTH EAST ASIA

Malaria:

Pathogen: plasmodium

Vector: mosquitoes

Host: humans and primates

Overall trend: as time increased, no. of cases of malaria treated and incidence rate decreased.

In order to reduce incidence and prevalence of malaria, prevention and control methods targeted the
mosquito vector:

Use of medicines targeted for malaria. Included:

o Primaquine removes dormant liver stages

o Chloroquine targets reproduction of bacteria, stopping it.

Decreasing mosquit larvae:

o Treating breeding sites of the mosquitoes with substances that kill the larvae
o Draining “still water ways”

Using insecticides to:

o Eliminate mosquito larvae by spraying indoor surfaces with them once or twice a year.
o Also using insecticidal nets qhich are sprayed with insecticies to provide physical and chemical barrier
agiant the, allowing for large-scale killing.

Reducing the likelihood of being bitten by:

o Using mosquito nests when sleeping

o Using replant
o Wearing long sovering clothing
o Using window screens,

7.4.6 EVALUATE HISTORICAL, CULTURALLY DIVERSE AND CURRENT STRATEGIES TO

PREDICT AND CONTROL THE SPREAD OF DISEASE

Historical:

o Poor hygiene causing infected wounds

o Believeing disease was caused by dead matter
o Quarantine
o Hospitals were strategically located with natural barriers to separate them from the population.
o Isolation of infected to control spread.

Culturally diverse strategies:

 o Traditional Chinese medicine (herbal tea, acupuncture)
o Traditional Indian (ayurveda)
o Herbs and spices with antibiotic properties, e.g. turmeric, ginger.
o Food sthat have medical benefits, e.g. garlic and onions lower BP (phillipines)
o Close proximity with dead bodies due to certain cultural prctcies and rituals enhanced spread
o Hygiene
o

Current stragiesL

o Immunisation
o Public health campaigns
o Proper snaitation of medical equipment
o Food handling procedures
o Garbage disposal

7.4.7 INVESTIGATE THE CONTEMPORARY APPLICATION OF ABORIGINAL PROTOCOLS IN

THE DEVELOPMENT OF PARTICULAR MEDICINES AND BIOLOGICAL MATERIALS IN
AUSTRALIA AND HOW RECOGNITION AND PROTECTION OF INDIGENOUS CULTURAL AND
INTELLECTUAL PROPERTY IS IMPORTANT, FOR EXAMPLE:

BUSH MEDICINE

o Made from herbal extracts and used in the maintenance of health as well as in the prevention,
diagnosis or treatment of physical and mental illness.
o Is part of the indigenous culture. It encompasses the natural environment as well as the spiritual world.
Bush medicines are still used to treat basic diseases and at times for first aid.
o Traditions in southern and eastern australia have largely been lost, but efforts are being made by
anthropologists to record traditions from aboriginals in central and north-western australia.
o Bush medicines serve as raw materials for some drugs that are developed using modern
pharmaceutical techniques. Such drugs are known as “Crude Drugs”

Examples:

Tea tree oil: antibacterial and antifungal properties, treats acne, lice, insect bites. Used through creams infused
with oils extracted from leaves.

Kakadu plum: antioxidants , treats colds, flu, headaches, source of vitamin C, applied/used through eating of the
fruit.

Witchetty grub: treat burns and wounds, used by crushing into paste and applying onto wound.
SMOKE BUSH IN WESTERN AUSTRALIA

o A group of native shrubs grown in coastal western australia.

o It has healing properties thus used in aboriginal medicine.
o It contains conocurovone, a property which has the potential to destroy low concentrations of HIV.
o When commercially successful, WA government and private pharmaceutical company would benefit
from profits.
o Indigenous bush medicine is regarded as intellectual property, but not currently adequately protected
by legislation and thus can be exploited by commercialism.