Causes of Infectious Disease: How are diseases transmitted?

CELL THEORY: All organisms are made of cells, cells are the basic unit of life, all
cells come from pre-existing cells. Germ theory: disease and decay are the product of living organisms.
 describe a variety of infectious diseases caused by pathogens:
Health state of complete physical, mental and social well-being.
Disease Any process/condition that disturbs the normal functioning of the organism forms signs/symptoms.
Infectious disease caused by pathogens and can be transmitted from one person to another.
Pathogen agent that causes disease or illness in a host (usually microscopic- live/reproduce at the expense of
(uni/multi/ the host causing disease by releasing toxins, damaging tissue or competing for nutrients). When
non- cellular). microbes are not in balance, they can become pathogenic e.g., prions, viruses (hijack the cell),
Classified based bacteria (archaea), protozoa (nucleus. No cell wall), fungi (filamentous/yeast) and microparasites
on size, cellular (multicellular parasitic animals): endoparasites/ectoparasites e.g., tick/flea.
nature.  Obligate pathogen: organisms that cannot survive for long outside of the human body.
 Opportunistic pathogen: is normally commensal but can cause disease when the host's resistance is altered.
Infectious Caused by an organism/infectious agent that get into the body and cause problems (contagious). Likelihood = pathogenicity/host defence.
communicable disease: can be transmitted from plant-plant or animal-animal.
Virulence factors Allow pathogens to inhabit its host more effectively e.g., antibiotic bacteria resistance.
Size: (biggest  smallest): microparasites, fungi, protozoa, bacteria, viruses, prions
PATHOGENS DISEASE TRANSMISSION DESCRIPTION
Non cellular/non-living: not composed of cells, need a host to grow/reproduce. Can be seen with an electron microscope.
PRIONS: contains no genetic material. Modified/ Creutzfeldt-Jakob disease Eating infected meat. Triggers normal into resistant prion protein
misfolded proteins of 200-250 amino acids long (humans) Contaminated medical (responsible for breaking down incorrectly
causes degenerative diseases of the nervous equipment. Organ transplant folded proteins). Brain tissue is destroyed,
system. Found in the brain/spinal cord. No cures. from infected individual individuals lose neurological function.
VIRUSES: have genetic material. Unable to Influenza- influenza virus Inhaling respiratory droplets Causes fever, coughing, sore throat, runny
reproduce without host. Have protective protein (coughing, sneezing, talking). nose, contagious respiratory illness.
coat (capsid). Attaches to cell, enters cells to make Tobacco mosaic virus Insect. Contact with infected Discolouration and mottled browning of
copies of itself (DNA makes copies of RNA). Uses disease caused by TMV. plant/ contaminated leaves.
host membrane to form their own lipids. equipment
Cellular: composed of cells e.g., meningococcal (bacterial) can be vaccinated against- severe.
BACTERIA: (unicellular) with cell wall. Tuberculosis Inhalation of shed bacteria. Primarily affects lung tissue. When active,
Prokaryotic. Reproduce asexually via binary fission. (mycobacterium Produces harmful highly contagious and presents with
Have bacterial DNA/plasmids. Some have a tuberculosis). toxins/chemicals. Direct/ persistent coughing and leads to significant
polysaccharide capsule protecting from host indirect. Forms endospores tissue damage. Growing concerns with rise
immune system. Good bacteria = lactic acid lying dormant for yrs. of antibiotic-resistant strains.
bacteria enhance lactose digestion. Fire blight (Erminia Insect. Contact with infected Affects all parts of pome fruit (apples and
amylovora) plant/contaminated tools. pears) plants, makes plant look burnt.
PROTOZOA: unicellular eukaryotic no chloroplasts Malaria caused by Bite from infected female High fever shaking chills and flu-like illness
or cell wall. Binary fission. Have flagella. plasmodium genus P. mosquito. caused by rupture of red blood cells and
falciparum. damage to blood vessels.
Phloem necrosis in coffee Insect vector feeds from Yellowing of leaves eventual root dieback
plants. infected plant and carries. and death of the plant.
FUNGI: uni/multi-cellular. Eukaryotic heterotrophic Tinea caused by Tinea Contact with infected skin Itchy white patches between toes, sore,
have a cell wall of chitin. Heterotrophic no pedis (athlete’s foot) scales/fungi in damp area. flaky.
chlorophyll. Moulds: composed of tubular Powdery mildew caused Wind or water borne. white powdery appearance (large numbers
filaments (hyphae) forming to make mycelium. by many hundreds of Contact with infected plant or of spores).
species. contaminated equipment.
MACRO ORGANISMS: Multicellular eukaryotic Endoparasite: taeniasis Contracted by cattle after Abdominal pain, loss of appetite and weight
visible to naked eye. Endoparasites: live in hosts caused by Taenia saginata ingesting tapeworm larvae. loss. Tapeworm segments area passed in
body (flatworm). Ectoparasites: live outside the (beef tapeworm) Contracted by humans after faeces. Rash and flu-like symptoms often
body (flea). Cause disease directly or as vectors ingesting undercooked associated with joint pain/weakness in limbs.
that transmit other pathogens. meat that contains Paralysis tick secretes a neurotoxin. Results
Helminths- worm-like organisms inside the Ectoparasite: lyme tapeworm. in loss of muscle control, difficulty breathing,
gastrointestinal system living off nutrients. disease, is contracted heavy salivation and unconsciousness. In
Reproduce via laying eggs maturing in host. from bite of an infected Bite from tick. animals leads to respiratory or heart failure.
Parasitic arthropods: invertebrates acting as a paralysis tick.
vector for diseases. E.g., fleas, lice, ticks. Mosaic virus diseases: Aphid/insect vector via Aphids are sap-sucking insects. They transfer
result of organism acting feeding. the virus between plants by eating from an
as a vector. infected plant before moving to a non-
infected plant. Causes irregular
colouring/shaping of leaves.
o investigating the transmission of a disease during an epidemic

Pandemic: a new disease or a new variant of a disease that has spread across a wide geographical area often worldwide.

Endemic: is a disease known to have a long-term presence in a specific region. E.g., malaria (cases mildly fluctuating).

Epidemic: outbreak of an infectious disease that spreads rapidly among many individuals (population) within a defined geographical area
within a short period of time. E.g., covid in its first instance. Causes of epidemic:
  Weather conditions: malaria increases in the tropical wet season because mosquitoes breed more successfully. Heavy rains are
linked to outbreaks of diseases transmitted via the faecal-oral route as they overflow the sewers contaminating water supplies/food.
 New pathogens appear: AIDS was recognised in 1981 having been transferred to humans from certain species of African monkeys.
 Old pathogens reappear: influenza virus occurs in a number of genetic “strains” which mutate and alter their “antigens”.
 Migration into new population: Europeans exploring/colonising America/Asia introduced measles to native populations.

Zika virus epidemic in Brazil is caused by the Zika virus. Symptoms: very mild- fever, rash and headache or no symptoms. The disease is
problematic for pregnant females as it can pass through the placenta to the baby and result in miscarriage, preterm birth or birth defects.
Transmission: zoonotic pathogen- primarily by the bite of an infected mosquito. Secondary: from mother to foetus. Zika was first identified in a
sick monkey in 1947. In 1952 the first reported human case was confirmed and it has subsequently been detected in nearly 90 countries. In
2016, the WHO declared a Zika virus epidemic in Brazil (an estimated 1-1.5 million infections occurred). By mid-2017, cases of the disease
dropped to zero, scientists believe it was due to a combination of seasonal weather patterns that impaired the mosquito vector, vigilant
control measures and a degree of herd immunity that results from the high levels of infections.

Modes of transmission of infectious diseases, including direct contact, indirect contact, vector transmission: involves carrying or transfer of a
pathogen from an infected host  non-infected organism. Mode relates to ability of pathogen to survive outside a host cell. The gut can act as
a reservoir for pathogens. For a disease to be spread it needs a host that is susceptible to the disease, a disease-causing pathogen and a mode.

Direct contact: transfer of the pathogen via exposure to infected skin or body secretions (physical contact between the host and a non-
infected organism). Contact between organisms that are not parent and child- horizontal transmission. Contact between offspring and parent-
vertical transmission. Physical contact: touching, sexual transmission: (infection with certain bacteria, viruses, or other microorganisms that
can be passed from one person to another through blood, semen, vaginal fluids etc. e.g., HIV), kissing, direct contact, prenatal or perinatal.
E.g., HIV, herpes simplex virus. Ebola: by a virus which is endemic in African fruit bats it is able to infect various other mammals including
humans who make contact with an infected animal. E.g., by hunting for bushfood.

Indirect contact: transfer of the pathogen to a new host via a non-living object (no physical contact). Infection occurs from a reservoir created
by the host outside itself (contaminated materials and surfaces/objects). A fomite is any object or substance that carries infection. Airborne
diseases (through respiratory droplets: sneezes contain tiny droplets containing millions of virus particles E.g., flu, mumps, measles, TB etc) are
concerning, difficult to control. They may also occur via a vector. Includes: airborne transmission, touching infected surface, contaminated
food, infected surgical instruments, vectors e.g., mosquitos.
 FAECAL-ORAL ROUTE: e.g., polio. Many pathogens infect or live in the digestive system, and they shed infective cells, spores, or eggs
in vast numbers in the host faeces. Primitive sewerage systems can contaminate local water especially in tropical weather.

Vector (living- vehicle- non-living) transmission: transfer of the pathogen via another organism such as arthropod (indirect) e.g., mosquitos,
sandflies, ticks (unharmed by can transmit the bacteria/virus when they bite the host; usually bloodsucking and transmits the pathogen during
a meal). Most common in warm, humid parts of the world where conditions for insect survival/reproduction are favourable e.g., malaria.

Design/conduct a practical investigation relating to the microbial testing of water or food samples: IV: source of water. DV: number of colonies
recorded. CV: equal volumes collected, same temperature and incubation time. Reliability: repetition/averaging of consistent results. To
improve accuracy could include technology to better count microbial colonies. Method: collect water samples from different sources in sterile
test tubes. Use sterile techniuqes to add each water sample to a different agar plate. Close and seal. Repeat 5 times for each sample. Incubate
all plates at 30 degrees for 1 week.

 investigate the work of Robert Koch and Louis Pasteur, to explain the causes and transmission of infectious diseases, including:

Koch’s postulates: criteria designed to establish a causal relationship between a pathogen and a disease. Been controversially generalized to
other diseases. Koch hypothesised that each infectious disease was caused by a specific pathogen. Highlighted transmission of infectious
disease occurs when an infected individual passes on the causative pathogen to a non-infected individual. E.g., examined sheep blood who
died from ‘anthrax bacteria’ which he isolated. This was then injected into a healthy sheep which developed anthrax.

1. The microorganism must be found in abundance in all organisms suffering from the disease but not found in healthy organisms.
(Later discovered asymptomatic carriers of cholera). Might also be very low in number/not visible.
2. The microorganism must be isolated from a diseased organism and grown in pure culture (doesn’t apply to pathogens incapable of
growing in pure culture e.g., viruses are incapable of growth alone). Vibrio cholerae was also isolated from healthy patients.
3. The cultured microorganism should cause disease when introduced (inoculated) into a healthy organism- same symptoms.
(Tuberculosis- not all organisms exposed to an infectious agent will acquire the infection- different immunity)
4. Microorganism must be re-isolated from diseased experimental host and identified as identical to the original causative agent.
Culture maintain (tissue cells, bacteria, etc.) in conditions suitable for growth.
Growth media Nutrient Broth. solution freed of microorganisms by sterilization containing the substances required for microorganism growth.
Host an animal or plant on or in which a parasite lives.
Opportunistic Infections: that occur more often/are more severe in people with weakened immune systems than in healthy people.
Pasteur’s experiments on microbial contamination: Pasteur performed his swan-neck flask experiments which disproved the theory of
spontaneous generation (life originated spontaneously from the non-living decaying and rotting matter) and clearly demonstrated that
microbes are airborne (microorganisms come from pre-existing micro-organisms) and could therefore be transmitted from an infected to a
non-infected individual. He proposed the germ theory which states that specific microbes are the causative agents of infectious diseases. This
assisted him in developing vaccines to chicken cholera, anthrax (He took 50 sheep and provided two doses of attenuated vaccine to 25 while
the other 25 sheep had no vaccine, exposure to pathogen, after 3 days the vaccinated sheep remained healthy and the rest died) and rabies.
Hypothesis: life doesn’t spontaneously generate but is airborne. Pasteur began with two swan-neck flasks containing meat broth, both were
boiled to kill any microbes present. They were not sealed and therefore were exposed to air.
1. Control: the swan neck remained in tack  no bacteria present.
2. The swan neck was removed, and contents exposed to air bacteria is present trapped at the base of the swan neck.
Assess the causes/effects of diseases on agricultural production: 20-40% of global crop production is lost annually to pests and diseases (cost
of over $300 billion). 20% of livestock is loss to disease (reduced productivity). These losses limit the availability of food, fibre and dairy
products. The growing food demands typically require a move to industrial scale farming practices. While these practices produce higher yields
of the desired product at a cheaper cost, large numbers of genetically similar animals and plants are kept in extremely close proximity to one
another increasing risk of disease transmission. Transportation of products globally increases the risk of disease transmission/outbreaks.

Plant- Panama disease: caused by a fungal pathogen Fusarium oxsporum found in the soil. Majority of bananas grown are propagated
asexually (chosen for their sweetness/size)- genetically identical placing crops at risk of disease outbreaks. 1950s: dominate crop of Gros
Michel cultivar was infected. The fungus enters the plants vascular tissue blocking the xylem and preventing water/nutrient transport causing
the plant to wilt and die. Late 1950s: Cavendish was found to be resistant to Panama disease while also producing higher yields (currently
constitutes 50% of the total world banana production and 99% of the worlds export market). An estimated 50 billion tonnes of Cavendish
bananas are produced globally each year, with export value of over 10 billion. In Australia, banana production is valued at over 450 million.
1989: a new strain Tropical Race 4 was discovered in Taiwan in a Cavendish banana crop, which has now spread around the world and has
been detected in Australia and all major banana-growing countries. It is anticipated that the world’s banana crops will be decimated in the
next decade if new alternatives are not developed.

Animal- Newcastle disease: highly contagious disease of birds (concerning to poultry industry- because there is high morbidity which has a
significant impact on poultry meat and egg productivity and therefore income revenue) caused by Newcastle disease virus (NDV)

 Symptoms: lesions on proventriculus/gizzards/duodenum, oral/nasal discharge, bright green diarrhoea, neurological impairment.
 Transmission: spread by other birds (problematic in battery cage farming), through droppings/secretions form infected birds.
 Prevention: NDV-free countries e.g., Australia, place restrictions on the importation of animal products from regions where the
disease is endemic. When outbreaks occur all chickens are killed.
 Economic impact: The Australian chicken egg and meat industries are valued over $825 million and $2.5 billion per annum
respectively. Even a small ND outbreak in Australia would impact significantly on the egg/meat industry (countries import from NDV-
free countries only). 2002-2003 outbreak in USA required the culling of over 3 million birds at an estimated cost of $230 million.

Fungi- Dry Bubble disease: is a fungal disease of commercially grown white-button mushroom caused by Lecanicillium fungicola. Symptoms:
late infections causing brown lesions. Early infections: deformed masses of undifferentiated mushroom tissue. Highly contagious with spores
spread easily through water and air. Grown asexually  low genetic variation (highly susceptible to outbreaks) BUT produces crops of great
quality/quantity. Australia produces over 70000 tonnes of mushrooms per annum ($450 million), while the global market is valued over $65
billion. Currently, dry bubble disease is estimated to cost the industry 5% of total annual revenue. Plastic bottles filled with salt kill the disease.

 compare the adaptations of different pathogens that facilitate their entry into
and transmission between hosts.

Case study 1: Plasmodium Falciparum (malaria): there are five species of protozoan
from the plasmodium genus that causes malaria (unable to survive outside host).

1. A female mosquito takes a blood meal (injecting with a proboscis) inoculating

human with sporozoite (motile spore-like stage) stage of P. falciparum.
2. Sporozoites migrate to liver via capillaries and infect hepatocytes (liver cell).
Sporozoites reproduce asexually by multiple fission to produce merozoites
(host cells rupture and merozoites break out of the liver and re-enter the
bloodstream, where they invade red blood cells, grow and divide further, and
destroy the blood cells in the process).
3. When in the RBCs the merozoites enter the next stage of the life cycle, called
a trophozoite. First, they can reproduce via multiple fission to produce more
merozoites (daughter pathogens) which cause the RBCs to rupture, releasing the merozoites into the bloodstream to repeat the
cycle (causes symptoms: fever, chills, sweats and anaemia). OR merozoites differentiating into either male/female gametocytes
(microgametocytes and macrogametocytes respectively).
4. The gametocytes are ingested by another female Anopheles mosquito during a blood meal where they mature in the digestive tract
of the mosquito to a form either a male gamete (microgamete) or female gamete (macrogamete).
5. The gametes fuse to form a mobile diploid zygote (ookinete) which migrates through the midgut wall and develops into an oocyst (a
resistant, thick-walled spore containing the zygote).

Adaptation to facilitate entry into the host: the infected female mosquito must first bite and penetrate the skin. To obtain a blood meal, the
mosquito releases an anticoagulant protein which prevents the blood from clotting and P. Falciparum exits the mosquito’s salivary gland.

Adaptations to facilitate transmission between hosts:

1. At each stage of pathogen’s life, different antigens are produced, preventing hosts from initiating an effective immune response.
 2. Once it has entered the red blood cells P. Falciparum produces adhesion proteins which are presented on the surface of the cell. The
proteins change the shape of the RBCS’s slowing their movement through blood vessels. This aids the merozoites in exiting the cell.

Influenza: Only influenza A has caused global pandemics. Symptoms can include fever, chills, headache, sore
throat and coughing and sneezing. Influenza A virus are categorises based on variations in two surface proteins:
haemagglutinin (H) and neuraminidase (N).

Adaptation of influenza to facilitate entry into host: The H and N surface proteins of the influenza virus have
evolved to bind to specific receptor proteins on target epithelial cells that line the upper and lower respiratory
tract. Once inhaled the virus quickly binds to host cells, where it is endocytosed before hijacking the cell’s genetic
machinery to replicate. While inside the host cell, it remains hidden from the host’s innate and adaptive immune systems.

Adaptations to facilitate transmission between hosts:

1. After the virus has reproduced within epithelial cells, it leaves the cells. As it exits the virus surrounds the RNA capsule with lipids and
glycans from the host cell. (avoids detection).
2. The influenza A virus has a high mutation rate (antigenic drift)- small rapid changes in viral genome and changes in the H and N
surface proteins (antigens) meaning the hosts immune system will not recognise the virus even if it has been encountered
previously. This results in ongoing transmission. Antigenic drift makes it necessary to develop annual vaccines.
3. Antigenic shift occurs when there is a new version of the H or N surface proteins introduced into the human population. (This
typically takes place when different influenzas virus strains infect an individual at the same time and swap gene segments in a
process called reassortment). The lack of recognition by the immune system results in rapid transmission of the virus and is
responsible for major influenza pandemics e.g., the 2009 swine flu pandemic.
4. Transmission is through inhalation of shed virus in airborne droplets. Symptoms of coughing and sneezing are highly effective at
transmitting the virus. Virus can remain viable on some surfaces for up to 2 days outside hosts.

Responses to Pathogens: How does a plant or animal respond to infection?

 investigate response of a named Australian plant to a named pathogen: 90% of plant diseases
are caused by fungal pathogens. Airborne fungal pathogens penetrate plant tissues via
openings (stomata/lenticels). Soil-borne fungal pathogens enter via the plants root system. All
plants have physical barriers (structural obstructions protect against microbe entry)/chemical
barriers (chemical characteristics that oppose microbe colonisation) that protect/slow
pathogens.

Fungal pathogens: Phytophthora dieback: is a soil-borne fungal pathogen that affects a wide range of
Australian plant species. 1940s-1970s: a significant outbreak of P. cinnamomi caused the dieback of Eucalyptus marginata over an area of
300,000 acres in Western Australia. Physical/chemical defence mechanism including cellulose and lignin in the cell wall which make the cell
difficult to penetrate AND secretes a range of antimicrobial chemicals e.g., like all eucalyptus E. marginata produces an oil (inhibits spread
through the plant tissues) which is stored in sub-dermal secretory glands prevent entry.

Cell and chemical mediated defences: E. marginata and P. cinnamoni case study.
 Gene for gene resistance: plants have resistance genes (R genes) that code for R proteins, which can bind directly with a specific
avirulence (AVR) protein that is coded for by an AVR gene (required for entry of a pathogen into a host cell). R protein interacts
directly with AVR protein. Once bound, the R-AVR complex prevents the pathogens from infecting new cells. R gene offers broad-
spectrum protection against any pathogen that produces the highly conserved AVR protein. No R gene = increased infection chances.
 Basal resistance: is trigged by the recognition of pathogen-associated molecular patterns (PAMPs) which are highly conserved
molecules common to various pathogens e.g., chitin. Plants can sense ‘self’ damage-associated molecular patterns (DAMPs) from
infected cells. The PAMPs and DAMPS are recognised by host pattern recognition receptors (PRRs) which result in fortification of
plant tissues. Cell junctions and stomata are closed restricting access to invading pathogens.
 Hypersensitive response (more effective if R-gene AVR gene complex is present- if basal resistance fails). Activated to restrict/stop
pathogens from spreading. Plant cells use chemical signalling to communicate the presence of a pathogen via protoplasmic strands.
The nucleus moves to the site of pathogen contact.  nucleus begins to disintegrate.  resin-like granules form in the cytoplasm +
spread throughout cell/fungus die (apoptosis).
 Systemic acquired resistance (SAR): non-specific, whole plant response that occurs once the HR has been triggered. Plant tissues
become highly resistant to a wide range of pathogens for an extended period. Pathogen binds to plasma membrane and induces a
signalling pathway (SP).  signalling pathway causes a hypersensitive response. Before the cells die, they release salicylic acid.
which is transported throughout the plant  leads to production of antimicrobial molecules (prep the plant for any pathogens).

analyse responses to the presence of pathogens by assessing the physical and chemical changes (both are non-specific- innate immune
response) that occur in the host animals cells and tissues

Innate immune system (first line of defence): the body has a range of non-specific physical and chemical barriers/mechanisms that work
together to prevent entry of microbes into the body that the organism was born with. Response is not improved with pathogen re-exposure.

PHYSICAL BARRIERS Description and location

Skin Upper epidermis contains keratin a protein that helps bind the skin’s cellular matrix making it
impenetrable to microbes (layers of dead, dry cells). Middle dermis contains hair follicles, sweat and
sebaceous glands (produce sebum, which seals the hair follicle preventing access by pathogens).
Hypodermis: bottom fatty layer of the skin and contains blood and lymph vessels (deliver cells
involved in the innate immune response if the skin is breached). It is a difficult environment for a
pathogen to grow on (no water). Skin flakes off, carrying microbes away.
Cilia Hair-like fibres off the epithelial cells which work with mucous membranes to direct trap microbes and sweep them out and away
from the body. Microbes are removed or destroyed via coughing or sneezing or encountering stomach acid after being swallowed.
Mucous membranes Line the respiratory (mouth/throat), urinary, and digestive tracts. Specialised epithelial cells (goblet
(muco-ciliary transport cells) secrete mucus (sticky fluid which traps pathogens) which lubricates the membrane and traps any
which disposes of/ejects microbes that enter the body. Microbes are then removed via various methods depending on their
particles and ‘germs’) location, sneezing, coughing, defecation, or urination.
Peristaltic waves of the digestive tract mix microbes with stomach acid and mucous membranes. Prevent microbial colonies from settling/infecting.
Urine flow (flushing Urine is passed under pressure during urination which removes any microbes present in the urinary tract. Urinary and
mechanism) reproductive openings are also slightly acidic (pH 6) which kills many microbes.
Microflora natural good bacteria which have a symbiotic relationship with humans (act as competitors for potential pathogens keeping the
population in check by outcompeting the pathogens or by creating chemical conditions that pathogens cannot tolerate).
Pathogens become opportunistic e.g., yeast Candida albicans when microflora is disturbed (Can Lead to Disease).
Reflex action Coughing and sneezing reflexes move dust, mucus and trapped pathogens out of the breathing passageways. Vomiting removes
stomach contents that are making you nauseous, removing pathogens which have been swallowed.
CHEMICAL BARRIERS Description and location
Acidic and alkaline Specialised stomach epithelial cells (parietal cells) produce hydrochloric acid (pH 1-2) which kills any microbes that enter via food
secretions or water. The duodenum has a pH of 7-8.5. Bile made in the liver is secreted into the duodenum where it neutralises acid entering
from the stomach and creates alkaline conditions. pH change is usually enough to kill any microbes that survive acidic conditions.
Sebum and sweat See skin. Sebum has acidic pH (4-6) making it an effective bactericide. Sweat has a slightly acid pH (6.5) which hinders bacterial
growth. Sweat also contains a protein called dermcidin which binds to bacteria and disrupts their function.
Cerumen (earwax) is high in fatty acids which lowers the pH to 4 which kills most microbes.
Lysozymes an enzyme produced by many animals (highly conserved). Degrades cell wall of bacteria by degrading peptidoglycan. This causes
bacteria to swell and burst due to osmosis- lyse (water moving into a bacterium). They are in salvia, tears, sebum and sweat.
Innate immune system: cellular/chemical responses: if a microbe breaches the barriers of the body, antigen molecules on the surface of the
microbes are recognised by the host as ‘non-self’ which initiates the innate immunes response (inflammation/phagocytosis).

Innate cellular responses: leukocytes (diverse group of cells- white blood cells that are involved in both the innate and
adaptive immune responses working to fight infections) involved in the innate immune response are either
granulocytes (neutrophils, eosinophils, basophils) which contain enzyme filled granules that damage/digest pathogens
after phagocytosis OR Monocytes which differentiate into either macrophages/dendritic cells, both are phagocytic
(engulf foreign bodies). (Note: red blood cells carry oxygen and are called erythrocytes).

Leukocyte Category Role

Macropha Acts primarily as phagocytes. Also release chemo attractants which activate other immune cells
ge and increase their migration to an infected site. Fixed macrophages are in tissues susceptible to
pathogen invasions (skin, lungs and intestine). Mobile macrophages circulate in the
Monocyte bloodstream and lymph system and are attracted to an infected site by the chemoattractant
molecules released by mast cells.
Dendritic Phagocytic antigen presenting cells (APCs) that express both major histocompatibility complex
cell (MHC) class 1 and 2 molecules on their surface. Bridges the innate/adaptive immune systems.
Circulate in the bloodstream where they capture and phagocytose pathogens directly or are
attracted to an infection site upon detecting chemo attractants.
Mast cell In all vascularised tissue. Stimulate vasodilation (blood vessels in the body widen) and vessel
permeability through release of histamine which leads to increased migration of macrophages
and neutrophils into infected area.
Neutrophil Phagocytic cells make up 50-60% of all leukocytes. Defend against smaller pathogens including
Granulocy bacteria, viruses and fungi. The death of neutrophils and tissue surrounding an infection site is
te visible as pus.
Eosinophil Defend against parasitic infections that are too large to be phagocytosed directly. Attach in a
group to the parasite and release digestive enzymes from their granules to destroy the
pathogen.
Basophil Can phagocytose. Primary role is the release of histamine (causes further vasodilation and
subsequent inflammation) and Heparin (prevents clotting from occurring too quickly which
would otherwise inhibit immune response).
Natural Granulocy Specialised white blood cell that can recognise body cells from viruses. Do not require prior
killer (NK) te activation and therefore play a central role in the innate immune system. Continually patrol the
cell (lymphocy body and can distinguish via the MCH 1 receptor pathway between healthy cells and pathogen
te) infected cells. NK cells will attach to virus infected cells and release chemicals that cause the
infected cell to undergo apoptosis. NK cells can also recognise some tumour cells.
Inhibitory receptors on NK bond to MHC1 on healthy cells, antigen not present  release cell. If
pathogen is present the MHC1 receptor on the target cell is modified and it binds to the
activating ligand of the NK cell.  Initiates release of cytotoxic chemicals e.g., digestive
 enzymes from the granules of NK cells.  causes membrane to degrade/apoptosis.
Inflammation response: occurs at the site of an infection/injury e.g., cut, abrasion, burn. Mast cells are
activated when their pattern recognition receptors (PRRs) detect the presence of pathogen-associated
molecular patterns (PAMPs) on the pathogen’s surface, which causes the degranulation of the mast cells and
release of proteases, prostaglandins and histamine- by mast/basophils (causes dilation of the blood capillaries
(and becomes more permeable) around the injury site allowing more blood/fluids to flow in bringing more
clotting factors and phagocyte cells (causing swelling/putting pressure causing drainage of fluid into the lymph
system- washing dead cell debris towards lymph nodes for disposal thus clearing the area), it also brings heat
to the site which can inhibit some pathogens and speeds up all chemical reactions for faster repairs). The mast
cells and fixed macrophages also release cytokines (interleukins/interferons) which attract phagocytes to the
site of infection. Cytokines coordinate the innate inflammation response and also the adaptive immune
response. Interleukins act as messenger molecules between immune cells while interferons are released by
infected cells, triggering surrounding cells to become more resistant to the invading pathogen. Interferons also
signal phagocytes and NK cells to target and destroy infected cells (causes pain and a fever).

When an organ transplantation occurs, the new organ cells act as antigens and set off an immune response- tissue rejection. To prevent,
doctors use only organs from donors who closely match the patient in tissue type or treat the patient with immunosuppressant drugs.

The innate immune response includes the secretion of many different proteins that aid defence. Some directly attack antigens while others
help trigger further immune responses e.g., lysozymes, proteins in the complement system can cause the cells of invading microbes to
burst/lysis, cells that have been infected release interferon (antimicrobial protein involved in response to viruses) which act beneficially on
neighbouring cells hindering viral replication.

Pathogens act as antigens (chemicals recognised as ‘non-self’) and so trigger the immune system as they have pathogen associated molecular
patterns (PAMP’s e.g., carbs, polypeptides, nucleic acids) and lack the self-proteins associated with host cells. Some pathogens replicate inside
cells (intracellularly) while others replicate outside the cells (extracellularly) e.g., in the blood or interstitial fluid.

Phagocytosis: phagocytes (neutrophils/macrophages/dendritic cells/eosinophils) engulf pathogens (when they detect antigens of a foreign
cell) via endocytosis and leaves them sitting inside a vessel/vacuole which merges with a lysosome (has acid hydrolase enzymes that digest the
contents of the cell, cutting the pathogen into tiny pieces and then releasing them via exocytosis). Opsonization uses opsonin’s to tag foreign
pathogens for elimination by phagocytes. Phagocytes can wrap around a pathogen/squeeze out of the bloodstream moving among tissue cells.

Complement system: (enhances ability of antibodies/phagocytic cells to clear microbes/damaged cells from an organism) a group of up to 30-
50 cleavable proteins (circulating through the bloodstream) that become activated when they encounter a pathogen (recognise an antigen).
Activation triggers a cascade (proteins cleaving other proteins) that coat a pathogen in complement proteins which enhances the binding of
antibodies to the pathogen and phagocytosis. Also increases inflammation. Some proteins act directly on the cell membrane of pathogen to
destroy them causing cells to lyse.

The lymphatic system: a network of delicate tubes throughout the body which drains fluid (lymph) that has leaked from the blood vessels
(plasma seeps out of the capillaries to bath the cells in tissue fluid keeping the cells moist for gas exchange) into the tissues and empties it back
into the blood stream via the lymph nodes, it also cleans the body system. Lymph tubes are one-way drainage system from all body extremities
to a point near the heart where tissue fluid is dumped back into a vein to re-join the blood. Tissue fluid is squeezed through by surrounding
muscles and the tubes have valves to prevent back flow. At various points along the lymph vessels there are lymph nodes (small lumps of
tissue containing white blood cells which fight infection, they filter lymph fluid composed of fluid and waste products from body tissues) which
traps fluids. If there is an infection, it is likely the pathogen will be carried along by the lymph fluid causing the pathogen to spread however
phagocyte containing lymph nodes generally prevent that. When fighting infections lymph nodes become swollen and painful.

Immunity: How does the human immune system respond to exposure to a pathogen?
Antibodies: IgM, blood proteins produced in response to encountering a specific antigen. Naturally produced by plasma B cells in
IgA, IgD, IgG, IgE response to antigen exposure (play a critical role in the immune systems defence). Specific antibodies bind to
(immunoglobulins specific antigens. Quaternary proteins consisting of four polypeptides: two heavy chains and two light chains
) joined to form a Y shaped molecule. The ends of the heavy and light chains form variable regions that are unique
to each antibody and act as the antigen-binding site.
Antigen Foreign substance/substances usually peptides/proteins recognised by the body/host as non-self and trigger production of antibodies.
Apoptosis when cells are so thoroughly infected, the area is sealed off and body cells are given a chemical instruction to ‘commit suicide’. Cells
(programmed cell produce enzymes to chop the cell DNA to pieces. Special antigens appear on the cell membrane which attract phagocytes to destroy
death) the cell/pathogen. Sometimes an affected site will be walled off by a layer of cells forming a capsule/cyst that isolates the infection.
Antigen Mediates the cellular immune response by processing and presenting antigens on their surface for recognition by lymphocytes e.g., T
presenting cells cells and provides a place for the helper T cells to dock.
B cells (activate are white blood cells that make antibodies, they’re in circulation in the blood. Have their own receptor bound antigens. Produce
humoral in/mature in bone marrow.
immunity)  Plasma cells: secretes immunoglobulin or antibodies.
 Memory B-cells: long-lived and quiescent cells that are poised to quickly respond to antigens.
Humoral immune (anti-body mediated immunity) Involves B cells and antibodies which deals with antigens from pathogens that are freely circulating or
response dealing outside the infected cells (extracellular antigens). Includes secreted antibodies, compliment proteins and certain antimicrobial peptides
with B cells/anti- located in extracellular fluids. Random processes create millions of variants of B cells, which have different antibodies on their
bodies surfaces. If a specific B cell has the right antibodies on its surface to bind an antigen, then the B cell becomes activated. It will then
proliferate/replicate by making many copies of itself. Some copies form plasma B cells which mass produced the same antibody while
 others differentiate and become memory B cells.
Cellular immunity is an immune response that does not involve antibodies. Rather, cell-mediated immunity is the activation of phagocytes, antigen-
specific cytotoxic T-lymphocytes, and the release of various cytokines in response to an antigen. (intracellular pathogens).
T-cells (produced They kill/ attack body cells that are infected by pathogens. If the pathogen is intracellular e.g., viruses. They are divided into:
in bone marrow,  CD4-helper t-cells: sense an infection and activate other immune cells to fight e.g., activates cytotoxic T-cells.
mature in thymus)  CD8 cytotoxic t-cells: immune cells that can kill certain cells (foreign cells, some cancer cells and cells infected with a virus)
 Memory T cells: trained to recognise specific antigens triggering a faster/stronger immune response.
 Suppresser T cells: reduce the activity of other T cells when necessary.
Immunisation intentional exposure to a pathogen to prevent infection. E.g., small pox survivors, created the concept of vaccination.
Lymphocytes are white blood cells uniform in appearance but varied in function and include T, B, and natural killer cells
Opsonization Immune response which uses opsonin’s to tag foreign pathogens for elimination by phagocytes. Antibodies and complement
components coat dangerous antigens to be recognised by antibodies or complement receptors on phagocytes. Molecules, microbes or
apoptotic cells are chemically modified to have stronger interactions with cell surface receptors on phagocytes and antibodies.
Cytokines Intercellular chemical messengers that initiate and constrain inflammatory responses to pathogens. Example: Interferon gamma:
critical to both innate/adaptive immunity. Functions as the primary activator of macrophages, stimulates NK cells and neutrophils.
Effector cells A cell that performs a particular function in response to a stimulus (have encountered a specific antigen and is involved in removal).
Memory cells circulate after the antigen has been eliminated. Memory cells initiate a quick immune response if the antigen is encountered again.
 investigate and model the innate and adaptive immune systems in the human body.
 explain how the immune system responds after primary exposure to a pathogen, including innate and acquired immunity.

Adaptive or acquired immunity (improved with re-exposure): immune responses that are developed (learned) and remembered against a
specific pathogen (produces an immunological memory of antigens encountered). Lymphocytic cells (B and T cells) are able to identify specific
pathogens by their antigens and adapt the defences to accurately target specific pathogens (will be destroyed in current and future infections).
Adaptative immunity is split into natural immunity is spit into passive (maternal- given to you naturally during development and post-natal
e.g., antibodies in breast milk) and active (infection) OR Artificial immunity is divided into passive (antibody transfer- purified antibodies,
naturalising agent) and active (immunisation). Adaptative immunity offers a rapid and highly effective response to specific antigens that have
been encountered.

Activating the adaptive immune system: all nucleated cells in the body express proteins on their surface (major histocompatibility complexes
class 1- MHC1). Each person has unique MHC 1 molecules, and this allows the cells of the innate
and adaptive immune systems to identify ‘self’ from ‘non-self’ antigens. If a ‘self’ cell has been
infected by a pathogen, it presents the foreign antigen on its surface via the MHC 1 molecules.
When an immune cell binds with the MHC 1 molecule, the foreign antigen is recognised, and an
immune response will result.

Antigen presenting cells (APC) e.g., macrophages, dendritic cells and B cells, also express MHC 2
molecules. After phagocytosis a pathogen is digested, and a portion of the pathogen is
expressed on the surface of the phagocyte via the MHC 2 molecule. The APC then migrates to
the lymph system where it presents the specific antigen to helper T (Th) cells via the MHC 2
molecule or to cytotoxic T (TC) cells via the MHC 1 molecule.  activates adaptive immune system. 
Th and Tc cells mature and proliferate.

Helper T cells activate the antibody-mediated (immunity) response. The Th cells bind (via their T cell
receptors) to the MHC 2 molecule of naïve B cells that are expressing the same specific antigen that
activated the Th cells. Th cells also release cytokines, promoting rapid clonal expression of the B cell
population specifically linked to the identified antigen.

Each naïve B cell contains a unique B cell receptor (BCR) capable of recognising a specific antigen. The
antigen is processed and presented on its cell membrane via MHC 2 molecules. The activated B cells
differentiate into memory B cells or plasma cells which act as antibody factories. The circulating
antibodies bind directly with antigens to form an antibody-antigen complex preventing them from
causing further infection and making them easier to recognise/be destroyed by phagocytes. Memory
B/T cells provide ongoing immunity as their receptors are specific to a previously encountered
antigen.

Cell-mediated immunity: antibodies are unable to bind antigens within a cell. As a result, the cell-
mediated immune response is required to target pathogens that have already infected host cells. This
process is regulated by T cells, which only recognise antigens when they are expressed on the surface
of an APC (via MHC2 molecules) or an infected cell (via MHC1 molecules). All T cells express a T cell
receptor- cluster of differentiation 3 (TCR-CD3) receptor complex which is required to bind both MHC
1 and MHC 2 molecules. The CD3 receptor is highly conserved while the TCR is highly variable to
account for different antigens. Different types of T cells are classified based on their additional surface
CD receptors. E.g., Th cells express CD4, and Tc cells express CD8 which are also required to bind MHC2
and MHC1 molecules of APCs respectively.
 The cell-mediated response is activated when an APC presents a specific antigen via an MHC 2 molecule to a complementary Th cell. The Th
cells then release cytokines to activate the mass cloning of Tc/Tm cells with receptors specific to the antigen. Activated Tc cells exit the lymph
system and migrate to the site of infection, where they bind via their specific receptor to infected cells presenting the antigen via their MHC1
receptors. The Tc cells degranulate releasing cytotoxins including perforin, which lyse the cell, killing any pathogen within it. T c cells perform a
similar function to NK cells with 1 difference: they require activation (adaptive immune response). Once an infection has been defeated,
regulatory T (Treg) cells are produced. Treg cells release cytokines that prevent further production of Tc
cells and B cells. Most circulating immune cells linked to the defeated pathogen die off, except for a
population of memory T and B cells (remain circulating or accumulate in the spleen/lymph system,
where they will rapidly proliferate to very large numbers if they are exposed to an antigen they have
encountered before).

Primary response: time taken to fight the infection is quite long (T/B cells have to be activated and
proliferate. Cytotoxic T cells need to kill the infected cells and for the B cells to produce plasma cells
that then secrete antibodies and bind with the antigen to neutralise it). Memory T/B cells specific to
the antigen are produced and remain in the body. Thus If the same antigen were to re-enter the body
in the future the secondary response, is much quicker. After identification of the antigen, the memory
cells will activate the production of the cytotoxic T cells and the B cells. Many B cells will then form many plasma cells, which secrete a much
larger number of antibodies than in the primary response (destroys the invading antigens before their numbers are large enough to cause any
symptoms).

Prevention, Treatment and Control: How can the spread of infectious diseases be controlled?
 Investigate/analyse wide range of interrelated factors involved in limiting local, regional/global spread of a named infectious disease.

Knowing the cause and transmission methods of infectious diseases allows government and health authorities to put in place appropriate
preventative and control measures to minimise spread. To limit the spread, contact between infected and non-infected individuals must be
kept to a minimum. Considerations measures to be implemented include: virulence of the pathogen, its incubation period, and population
density + mobility. COVID-19 (caused by viral pathogen SARS-CoV-2): In 2020, the WHO identified a ‘novel’ virus that caused pneuma-like
symptoms in fewer than 100 individuals in Wuhan, China. Soon after the disease was identified, the number of new infections and deaths
started to grow exponentially. Chinese authorities placed Wuhan and surrounding regions into strict lockdown, quarantining 20 million people.
By late January the virus had been detected in Europe, Asia and the USA. COVID-19 met the 3 criteria to be categorised as a pandemic: illness
resulting in death, sustained person-to-person spread, worldwide spread. In under two years global infections reached 350 million.
Local (most Forced two-week quarantine for individuals returning from overseas, fines for breaches. Forced lockdowns, mandatory mask wearing in all
specific) public spaces, night-time curfews, and travel bubbles where enforceable. ‘Pop-up’ testing and tracking facilities. Mandatory vaccination
required for certain professions. Proof of vaccination required to enter businesses/public facilities. Measures were monitored/enforced.
Regional ‘Hard’ border lockdowns to restrict movements within/between states. Extended lockdowns with heavy restrictions on the liberties and
movement of residents. Government approval/permits required to travel into regional areas. National Cabinet formed to address the
specific health and economic needs of each state. Staged approach to the vaccination rollout, with elderly and vulnerable populations
prioritised. Financial incentives provided to support people forced into unemployment. ‘No jab, no play’/‘No jab, no pay’ legislation.
Global WHO: responsible for the global governance of health/disease. It directly communicates with policymakers at the national and regional
levels to inform them of trending disease patterns. It also recommends and supports specific strategies to limit disease spread. E.g.,
Mathematical modelling to track and predict spread to the different virus variants (allowed regions to be proactive). Coordinated approach
involving thousands of scientists and public health authorities, to produce and distribute vaccines (within 18 months multiple companies
had produced vaccines). Planning/building of emergency operations centres, training of health workers, financing of vaccination programs.
 investigate procedures that can be employed to prevent the spread of disease, including but not limited to:

Hygiene (conditions/practices that assist in maintaining health/prevent disease spread) practices: either kill microbes or reduce the likelihood
of an infected person passing on the pathogen. Prior they didn’t have hygiene practices e.g., doctors wore the same pus-smeared gowns.
Level Details Examples
Personal Practices individuals can do to maintain good health and e.g., handwashing after defecating/before eating/handling food, bathing,
minimise the risk of becoming infected/infecting others. correct respiratory hygiene when coughing/sneezing, sexual protection.
Domestic Practices done at the household level to minimise disease e.g., keeping raw/cooked foods separate, cooking food for the appropriate
spread/focusing on food storage and preparation. time/temperature, storing food correctly, clean water for cooking.
Community Large-scale infrastructure programs that focus on providing e.g., water treatment/purification (filtration/chlorination), sewerage removal
society with access to clean water/food/sanitary conditions. and treatment, correct animal husbandry, maintenance of hygiene in markets.
Quarantine: period of strict isolation to prevent the introduction/spread of diseases or unwanted animals, plants, and pests into the country or
across state boarders. Prevents infected individuals from encountering non-infected individuals. Quarantine period: for a period in which a
pathogen is communicable. Australia remains free of many significant human and agricultural diseases, because of natural water barriers,
strict international/interstate quarantine regimes. Biosecurity strategies that complement quarantine are border inspections, enforced
destruction of diseases animals and plants and banning the importation of organic products
from most countries. All practices are essential in protecting Australia from serious
communicable diseases and economic loss. E.g., Australia is free from foot and mouth
disease (which could devastate sheep/cattle herds), malaria and sorghum downy mildew
(fungal pathogen with potential to destroy cereal crops/native grasses).

Vaccination (process of making people (or animals) resistant to diseases caused by specific
pathogens) including passive and active immunity:
Active immunity: occurs when activated B cells differentiate into plasma cells and antibodies are produced. This can occur naturally when an
individual is exposed to a pathogen (becoming ill and recovering- danger is the person might not survive) or artificially through vaccination.
Vaccines works by exposing the immune system to a compromised version of a pathogen (inducing a primary immune response without
symptoms) which then activates the adaptive immune system, leading to the production of antibodies and memory B and T cells specific to the
antigen (provides long-term protection from the disease). If a secondary exposure occurs the immune response is faster and stronger due to
the presence of circulating antibodies and memory B and T cells generated from the primary exposure (more effective elimination of the
pathogen). Common active vaccines contain:

 a live attenuated (weakened version of the pathogen (e.g., measles, and chickenpox vaccines)
 an inactivated (dead) version of the pathogen (e.g., hepatitis A virus vaccines)
 viral messenger RNA (mRNA) (e.g., some COVID-19 vaccines)

Passive immunity: involves an individual receiving antibodies not produced by their

own immune system. Natural: from mother to foetus via the placenta or from mother
to newborn during breastfeeding (temporary and starts to decrease after being born) or
Artificial: through vaccination where antibodies are injected directly into an individual
(e.g., certain diphtheria vaccines i.e. blood fractions containing antibodies). Passive
immunity provides an immediate protection against a disease however because no
memory B or T cells are produced, the protection is short-lived and booster shots must
be given if an individual is deemed to have been at risk of exposure.

Herd immunity: some individual cannot be vaccinated because of age-related or health

reasons. When a significant majority of individuals are vaccinated (around 90%) unvaccinated individuals are also protected as there are fewer
hosts available for the disease to spread between.

Public health campaigns (use media platforms to disseminate information to reach audiences): seek to provide community members with the
necessary information to have them engage in behaviours that improve their health and prevent the spread of infectious diseases. e.g., 1980s
public health campaign to raise awareness about HIV-AIDS included TV commercials in which the Grim Reaper killed people with a bowling
ball. The campaign was graphic and highly effective and in conjunction with many other initiatives resulted in the incidence of new cases falling
in subsequent decades. National COVID-19 public health campaign: spread across all forms of media including daily updates of new infections
and deaths, health experts highlighting the importance of vaccination and television advertisements showing people who had contracted the
disease, to promote uptake of the vaccination program. These contributed to round 90% of eligible Australians receiving double vaccinations.

Use of pesticides: help to prevent the spread of infectious animals and plant disease. These chemicals target pathogens and insect vectors that
carry pathogens. While there is still widespread dependence on pesticides, there is also growing awareness of the impact they can have on
people’s health and the environment. Genetic resistance is also developing; thus pesticides need to continually be developed, or alternated.

Genetic engineering: intentional modification of an organism’s genome to alter its phenotype. It is valuable in
agriculture because of the growing resistance of pathogens and insect vectors to traditional chemical treatments. E.g.
Cotton Bollworm which chews holes in cotton plants and have evolved resistance to pesticides. Scientists have
transferred the soil bacterium into a plant’s genome for the production of a toxin which is lethal to the caterpillar if
eaten creating a transgenic species. CRISPR-Cas-9 has been used to genetically sterilise male Anopheles mosquitoes
(vectors for pathogens e.g., malaria). When the males mate, this causes the wild-types female to become infertile.
 Investigate/assess effectiveness of pharmaceuticals as treatment strategies for control of infectious disease:
Antivirals- off target negative effects (inhibiting the hosts production of polypeptides) (aim to prevent viral particles
entering or developing within the host cells they invade): viruses are non-living pathogens. It consists of nucleic acid
(either DNA or RNA) encased in a protein coat (capsid). Some viruses are also enclosed in a second protective layer-
envelope (consists of lipids derived from the host cell’s membrane and viral proteins that play a role in infecting new
cells). DNA viruses cause hepatitis B and herpes. RNA viruses cause HIV and COVID-19. Viruses require a host cell to
reproduce, thus there are significant challenges to developing antiviral drugs. Any attempt to target the virus
inevitably causes death or damage to the host cells, never producing a cure rather suppressing rate of viral replication
by:
 Inactivation of the capsid or envelop proteins, which inhibits viral attachment to the host cell.
 Inhabitation of transcription and translation during viral protein synthesis.
 Inhibition of new viruses being released from host cells.
This inevitably results in rapid development of drug resistance. Antiviral medications are effective at reducing symptoms and sometimes
extending the life of infected individuals. A decreased viral load also reduces the risk of transmission. However, the specificity of antiviral drugs
and the high mutation rate of viruses (RNA viruses- up to 1 million times higher than that of the host) make most drug development options
economically non-viable.

Antibiotics (substances produced by microorganisms/chemicals which are specific for bacteria which kill or inhibit the cells of microbes but do
not harm human cells helping to control diseases): are categorised as either bactericidal (kill bacteria by interfering with the formation of the
cell membrane, cell wall or cell contents e.g., penicillin- during reproduction prior to fission of bacteria (penicillin
inhibits the enzymes that cross link weakening the cell wall which bursts and releases the cytoplasm- don’t kill body
cells as they lack a cell wall) or bacteriostatic (inhibit bacterial growth by interfering with DNA replication and protein
synthesis. They do not kill the bacteria and therefore rely on the immune system to clear the infection e.g., amoxicillin).
Both groups have broad-spectrum (antibiotics are effective against a wide range of bacterial species- can be used when
the causative pathogen is suspected of being bacterial without the actual species being identified) and narrow-spectrum (antibiotic is highly
specific and acts only on a very small number of bacterial species) examples. Antibiotics target cell structures and molecules not found in
humans e.g., the cell wall or prokaryotic ribosomes. They do not affect host cells and therefore have very few side effects. However, the
overuse and misuse of antibiotics has lead to the evolution of ‘superbugs’ bacteria which are resistant to antibiotics (bacteria treated with
antibiotics- variants with the genes that protect them are able to survive and reproduce- resistance via spontenous mutation- vertical
evolution and exchanging genes- horizontal evolution). E.g., drug-resistant forms staph infections.
 Disadvantages: Data indicates that bacterial resistance to antibiotics is increasing and so the concern about development of
resistance is real and problematic, Resistance in less dangerous strains of bacteria can be transferred to more aggressive types,
previously used antibiotics are no longer effective against some strains of bacteria (e.g. gonorrhoea), Infections that have been able
to be controlled now pose a threat, Pressure on drug companies to research and develop new drugs - an expensive/time consuming.
 investigate and evaluate environmental management and quarantine methods used to control an epidemic or pandemic.

Epidemic: Is an outbreak of infectious disease within a defined geographical area that spread at a rate above what is normally expected.

Pandemic: spread of new disease or a new variant of a disease, across a wider geographical area, often worldwide.

Controlling disease spread during epidemics/pandemics is to prevent contact between infected/non-infected individuals using environmental
management (provision of clean water/food appropriate sanitation/personal protective equipment/maintain good air quality)/quarantine
methods (isolate infected or exposed individuals for the communicable period, combined with environmental management).

CASE STUDY: COVID 19 (SARS-COV-2)- spread of COVID in Australia was initially prevented through a range of environmental management/
quarantine methods- (‘pop-up’ testing facilities to test, track and isolate infected individuals, forced lockdowns, mandatory mask wearing in
public spaces has been reduces the spread of exhaled aerosols up to 80%, and social distancing (combined with mask wearing increases up to
90%) became central to slowing the spread of the virus until the vaccine rollout- 2021), however flaws in biosecurity ultimately lead to the
significant COVID-19 outbreaks in NSW and Victoria. Highly effective- drop to near zero new cases in Victoria after lockdowns 1 and 2. Of the
nearly 2000 COVID deaths in Australia between 2019 and 2021 the majority were unvaccinated and the 11.7% who had been double
vaccinated all were elderly or had significant health issues. While individuals can still contract COVID after being vaccinated the risk of
becoming seriously ill is reduced significantly with only 1.9% of intensive care unit patients being double vaccinated. There was a drop in
incidence/mortality in March/August 2020 resulted of forced lookdowns and restrictions limiting people’s mobility. Vaccines and eased
restrictions, there was a high incidence rate that was not mirrored by increased mortality.

Impacts of different stakeholders (lockdowns/movement restrictions on economy): 158 billion losses, mental health impacts, concerns about
civil liberties (do forced lockdowns restrict movement/mandatory vaccinations infringe on individuals’ rights?) versus the greater good and the
burden that unvaccinated individuals will place on the health care system (hospitalisation). This may prevent vaccinated individual from
receiving medical treatment for other often serious health conditions.

 interpret data relating to the incidence and prevalence of infectious disease in populations, for example:
Mobility of individuals (important consideration when considering risk assessment of disease transmission e.g., movement within
regions/states/international against incidence/prevalence rates determines what limitations need to be imposed on a population to reduce
transmission) and the portion that are immune or immunised: Prior to vaccines, incidence/mortality reduction was attributed to force
lockdowns/restrictions that limited people’s mobility. The vaccination rollout commenced in Feb 2021 (end of 2021 national average of
individuals who were fully vaccinated was over 90%). This came with a significant easing of the restrictions that had limited people’s mobility
which increased the incidence of new COVID-19 cases. Limiting mobility reduced the spread of the disease while vaccinations reduced the
number of deaths.

Malaria/Dengue Fever in Southeast Asia: WHO estimates that the global prevalence of new malaria cases was 200-250 million per annum for
the past two decades (overall downward trend in case numbers). Mortality rates with a fall from 736000 in 2000 to 204000 in 2019. Of the 87
countries where malaria is endemic, nine (Bangladesh, Bhutan, India, Indonesia, Maldives, Myanmar, Nepal, Sri Lanka and Thailand) are in the
south-east Asia region with cases contributing to approximately 3% of global malaria burden. Between 2000-2019 the annual prevalence in this
region dropped from 23 million to 6.3 million while the incidence dropped from 18.1 cases to 3.9 cases per 1000 of at-risk population. While
decreases in prevalence and incidence of malaria occurred in all 6 WHO region, the drop was most significant in South East Asia. With 25% of
the world’ population in Southeast Asia, the WHO has actively targeted the region with financial support and a range of national malaria
elimination programs.

Mobility:

Incidence: number of new cases of a disease in a population in a specified time period. Used to examine how quickly a disease is spreading
through a population. Governments/health authorities can use this data to make decisions on how best to intervene/reduce transmission.
number of new cases during a specific time
× 100.
¿ population at start of monitering period
Prevalence: total number of disease cases in a population in a given period of time. Determines likely burden outbreak will cause for health
facilities/society. Influenced by incidence, period of illness/infection and morality.
total number of new cases during a specific time
×100
¿ population at start of monitering period
 evaluate historical, culturally diverse and current strategies to predict and control the spread of disease.
Prior to the germ theory, predicting and controlling disease spread was largely dependent on observed correlations between specific
behaviours /environmental conditions and disease outbreaks. In response, practices were introduced to minimise contact between infected
and non-infected people. After germ theory, specific pathogens and their mode of transmission could be linked to a particular disease
improving prediction/disease control.

Historical: lack of scientific knowledge meant cultural values/beliefs influenced more e.g., the bubonic plague which killed 25+ million people
was attributed to the wrath of God punishing sinful behaviour. This view resulted in limited success predicting/controlling outbreaks.
 Late 14th century: link was made between the plague/movement of symptomatic people. Response: quarantine was introduced in
European ports to reduce transmission of the disease. Ships were required to remain at anchor for 40 days before crew could leave.
 Mid-1840s, Ignaz Semmelweis: early antiseptic procedures including handwashing prior to performing medical procedures making
the connection between women dying during childbirth from puerperal sepsis, a bacterial infection of the reproductive tract and
doctors delivering babies after performing autopsies on cadavers. He predicted mandatory handwashing/antiseptic procedures prior
to childbirth would reduce morality rates. Women had a 20% chance of dying during childbirth. After the procedures: less than 2%.
 In 1854, Doctor John Snow mapped the number of cholera (water borne disease) cases in the public water well. He determined that
the cause of the outbreak was a contained water well. His discovery was significant as it provided the first indication that cholera
could be controlled by providing and maintaining clean water sources. Snows collection and analysis of the data is one of the first
recorded examples of an epidemiolocal study.

Cultural strategies: culture- ideas, customs and behaviours of a group of people. Cultural beliefs can contribute to the prevention and control
of disease spread. e.g., for over 4000 years, Greek, Roman and Chinese cultures disinfected water by either boiling or charcoal filtration (iron
particles attach to dirt/pathogens)- the link had been made between consumption of dirty water and disease. Some cultural practices can
promote spread of infectious disease e.g., in West African countries burial ceremonies involve direct contact with the deceased individual
(Ebola virus: transmitted through bodily fluids and is highly contagious with a morality rate of 90%). The epidemics were brought under control
through a range of initiatives including improved public health and education campaigns, contact tracing and the enforcement of safe burials.

Current strategies: the WHO uses satellite imagery and global climate patterns to develop models that can be used to track and predict the
spread of seasonally linked diseases e.g., malaria, and zika virus allowing control measures to be implemented prior to the outbreak to reduce
transmissions. R0 value is an indicator of how contagious an infectious disease is determined by the infectious period, contact rate and mode of
transmission (number of new individuals a continuous person will infect in 24 hours). It is used to predict whether an epidemic or pandemic is
spreading and whether control measures are working. The goal is to reduce R0 to less than 1 (declining, 1 is stable).

 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:

Bush medicine: historical/traditional use of native Australian plants for both physical/spiritual healing by Indigenous Australians for over
50,000 years. Research into bush medicines has discovered active ingredients e.g., anti-canner and antiviral properties. Pharmaceutical
companies seek to patent the active ingredient to ensure long-term financial benefit from their research. This raises ethical and legal
considerations as to who has legitimate ownership of the intellectual property, given that Indigenous Australians have used the product for
thousands of years, albeit without knowledge of the active ingredient.

Smoke bush in Western Australia: in the 1960s, the Western Australian government awarded a license to the US National Cancer Institute to
screen native Australian plants for compounds with anti-cancer effects. None were found, but the plants were tested again in the 1980s and
smoke bush (Conospermum stoechadis) was found to contain an active ingredient, conocurovone that could destroy HIV in low concentration.
In the 1990s an Australian pharmaceutical company was awarded an exclusive licence to develop the patent for a conocurovone-based drug to
treat HIV. The projected royalties if successful were estimated at $100 million per year. Indigenous Australian people were not consulted about
the collection and testing of plants from Country and received no financial benefit or acknowledgement from the project, despite the cultural
importance of the plant and their knowledge of its medicinal properties.

Kakadu plum: (terminalia ferdinandiana) found in northern Australia. Indigenous people local to the region have used the fruit of the Kakadu
plum for over 40000 years as a source of food and for its natural healing properties to treat colds, flu and headaches. Extracts were used as an
antiseptic balm to treat ailments e.g., rheumatoid arthritis and fungal and bacterial infections. Kakadu plum as has the highest vitamin C of any
fruit and strong antioxidant properties that support the immune system in fighting infections and prevents scurvy (nutritional disease). Studies
also indicate that the fruit is a high source of gallic and ellagic acid which have been linked to a range of health benefits, including anti-cancer,
anti-inflammatory and antimicrobial effects. Several pharmaceutical and cosmetic companies have lodged patents to gain exclusive licensing
rights to the research and any economic benefit derived from the fruit. E.g., in 2010 a US company Mary Kay applied to patent the gallic and
ellagic acid extracts from the Kakadu plum. The cosmetic company sought to use these active ingredients for their antioxidant properties and
ability to repair damaged skin and reduce collagen breakdown. In 2021, Mary Kay withdrew the patent application due to concerns raised by
local Indigenous Australian representatives regarding their ongoing access and use of Kakadu plums. Another factor was tighter government
regulations which were introduced in response to a similar case that occurred with smoke bush in WA.

Indigenous Cultural and Intellectual property (ICIP) laws are now in place to protect against the exploitation of traditional arts and culture of
Aboriginal and Torres Strait Islander peoples creating an appropriate balance between competing interests. Any financial benefits gained from
research into bush medicines must now be shared with nay Aboriginal or Torres Strait Islander communities.