Module 7.

Infectious Disease

7.1 Causes of Infectious Disease

Describe a variety of infectious diseases caused by pathogens, including

microorganisms, macroorganisms and non-cellular pathogens

Pathogens and infectious disease

●​ A disease is any condition that adversely affects the function of any part of an organism.
●​ A pathogen is a disease-causing organism.
○​ Cellular (bacteria, fungi, protozoa, macroparasites)
○​ Non-cellular (viruses and prions).
●​ An infectious disease is any illness caused by a pathogen, and that can be transferred
between hosts.

Cellular pathogens that cause disease in plant and animals

Bacteria
●​ Description: Unicellular prokaryotes, lack
membrane bound organelles
●​ Size range 0.5 - 5 μm
●​ Bacilli (rod); Cocci (spherical); spirochaetes
(spiral); vibrio (curved rod)
 ●​ Reproduction: binary fission (mitosis), replicate in vacuole or cytosol and spread,
intracellular take over protein synthesis mechanisms
●​ Transmission: skin contact, bodily fluids, airborne particles, contact with feces, and
touching a surface touched by an infected person, release toxins harmful to host, invade
body, reproduce and grow in tissues
●​ Immune response: increasing local blood flow (inflammation) and sending in cells from
the immune system to attack and destroy the bacteria. Antibodies produced by the
immune system attach to the bacteria and help in their destruction.
●​ E.g: streptococcus, cholera, food poisoning, gastritis, pneumonia
●​ Treatment: Antibiotics (disrupting the bacterium’s metabolic processes) , Broad
(Amoxicillin), Narrow (penicillin)

Fungi
●​ Description: Unicellular or multicellular eukaryotes, often found in soil or on decomposing
organic matter
●​ Filamentous fungi have long branching threads called hyphae
●​ Reproduction: Asexually, fragmentation, budding, spores
●​ Transmission: Produce microscopic reproductive spores that are spread through air,
water, direct contact. Humans infected mostly on skin, nails, hair
●​ Immune response: possibly an allergic reaction e.g. sneezing, coughing
●​ E.g. thrush, tinea, asthma
●​ Treatment: antifungal creams, sprays, tablets

Protozoans
●​ Description: Unicellular eukaryotes of the protista kingdom
●​ Get food from environment including water, soil and human body
●​ Size range: 2 - 1000 μm
●​ Reproduction: binary fission as well as sexual
●​ Transmission: Cyst stage (dormant) infect humans - Trophozoite stage (active, feeding,
reproducing) disease develops
●​ Plasmodia spread by anopheles like mosquitoes, reproduces in RBC and released into
bloodstream
●​ E.g. plasmodium (causes malaria), sleeping sickness
●​ Treatment: antibiotics, sulphur medications

Macroparasites/macroorganisms
●​ Description: Multicellular eukaryotes that are visible to the naked eye
●​ Can live internally or externally (endoparasites vs ectoparasites)
●​ Reproduction: Live and grow inside host; reproduce outside host
●​ Transmission: Mostly live in the human gut. Lay eggs that pass in faeces to the
environment, eggs develop into larvae and re infect humans through food. Move into the
 bloodstream and are transported around the body often back to the gut where adults
continue the cycle.
●​ Immune response: sometimes high temperature
●​ E.g. tapeworm, ticks, fleas
●​ Treatment: improved sanitation, education, living conditions, also medication

Non - Cellular pathogens that cause disease in plants and animals

Viruses
●​ Description: DNA or RNA (nucleic acid) enclosed in a protein coat used to recognise
suitable host cells
●​ Non-living; can only reproduce inside host cells
●​ Size range: 20 - 300 nm
●​ Reproduction: Once attached to a host cell, a virus injects its nucleic acid into the cell.
The nucleic acid takes over the normal operation of the host cell and produces multiple
copies of the virus's protein coat and nucleic acid.
●​ Transmission: droplets that fly out when you cough or sneeze, land on the mouths or
noses of others nearby, touch mucus droplets from someone
else on a surface like a desk and then touch your own eyes,
mouth, or nose before you get a chance to wash your hands.
Viruses like the flu can live 24 hours or longer on plastic and
metal surfaces
●​ Immune response: Pyrogens produced, raise body temp, slow
chemical reactions (White cells produce antibodies to stop virus
replication)
●​ Cytotoxic T cells have specialised proteins on their surface that
help them to recognise virally-infected cells. These proteins are
called T cell receptors (TCRs). Each cytotoxic T cell has a TCR
that can specifically recognise a particular antigenic peptide
bound to an MHC molecule. If the T cell receptor detects a
peptide from a virus, it warns its T cell of an infection. The T cell
releases cytotoxic factors to kill the infected cell and, therefore,
prevent survival of the invading virus
●​ E.g: influenza, Covid-19, cold, HIV, ebola
●​ Treatment: Vaccines, (polio, measles, chickenpox, flu, hep, HPV), also antiviral
medications

Prions
●​ Description: Misfolded proteins in cell membrane
●​ Distorted shape which induces distortion of normal proteins
●​ Can be both infectious and hereditary (unique)
 ●​ Cause group of progressive degenerative neurological diseases in mammals called
transmissible spongiform encephalopathies (TSE)
●​ Transmission: Pathogen prions infect lining of neural cells which are destroyed and lead
to the infection of others, from eating infected meat, surgery with contaminated
instruments, corneal transplants, growth hormone injections
●​ Response: No immune response as prions resemble proteins normally found in the body
●​ E.g. CreutzfeldtJakob Disease (CJD or mad cow disease), kuru
●​ Treatment: none

Infectious protein (prion) has an unusual shape allowing it to bind

to the normal form of the protein.

Upon contact, the prion induces the normal protein to fold

incorrectly

The original and newly formed prions attack other normal proteins
nearby. This continues until the prions accumulate to lethal levels
where symptoms are evident.

Compare the adaptations of different pathogens that facilitate their entry into and
transmission between hosts

In order for a pathogen to be able to cause disease, it must:

1. Gain entry to the host

2. Reproduce in host tissues
3. Avoid the host's defences
4. Cause harm to the host

Portals of pathogen entry

Gastrointestinal tract
●​ Food contaminated with microorganisms
 ●​ Often destroyed in stomach
●​ Eg. holera, typhoid fever, mumps, hep A

Respiratory tract
●​ Airborne viruses which are inhaled from other peoples’ expelled mucus
●​ Eg. diphtheria, meningococcal meningitis, tuberculosis, whooping cough, influenza,
measles, chickenpox

Trade-off hypothesis
●​ Viruses are evolved to maximise the overall success by achieving balance between
replicating host (virulence) and transmitting to other hosts

Urogenital openings
●​ Entry points for STDs and other infection
●​ Eg. thrush, gonorrhea, syphilis, HIV/AIDS

Breaks in skin surface

●​ Easy entry for pathogen
●​ Some have adaptations allowing for penetration of skin surface
○​ Eg. tetanus, gas gangrene, bubonic plague

Pathogen adaptations: virulence factors (aid or enhance the microbes ability to invade and
spread within the host)
●​ Adherence: in order for a microbe to cause disease, must first adhere to the host
surface. Some microbes produce adhesive materials and escape defences
●​ Pili : involved in attachment and gene transfer in bacterial conjugation
●​ Fimbriae: thinner, shorter, less rigid, more numerous
●​ Neisseria gonorrhoeae , if a strain has no pili it is not. The chemicals that allow such
attachment are called “ adhesins' ' They are often glycoproteins or proteins that bind to
receptors on host cell surfaces.
●​ Glycocalyx - capsule is a tightly bound polysaccharide material on the outside of certain
bacterial cells (part of a bacterial envelope)
●​ Spikes - viral envelopes of some viruses

Adhesion
●​ Process of microbes sticking to surfaces
●​ Key initial first step
●​ Adhesins

Surface molecules on pathogen (adhesins or

ligands,) bind specifically to complementary
surface receptors on cells of certain host
tissues
 Infection

●​ Enzymes are released that digest the connective tissue of the host, allowing the spread
of infection
●​ Metabolites released to destroy phagocytic white blood cells
●​ Enzymes released to break down fibrin (threads of protein deposited when blood clots to
limit movement of pathogens

Adaptation by method of transmission

Airborne transmission adaptations

●​ Pathogens resist drying out
●​ Pathogens cause sneezing and coughing
●​ Able to tolerate a wide range of O2 concentrations

Waterborne transmission adaptations

●​ Outer surface structures (e.g. fimbriae) assist with motility
●​ Pathogens are often halotolerant (can tolerate high salinity)
●​ Many are not destroyed by boiling of the water

Vector-borne transmission adaptations

●​ Life cycle of pathogen is synchronised with feeding habits of hosts

Faeco-oral transmission adaptations

●​ Pathogens are stable in varied environments (e.g. acid in stomach, low O2 in large
bowel)
●​ Pathogens often induce vomiting and diarrhoea to increase transmission rates

Adaptations of bacteria

Adhesion
●​ A fimbria is a type of pilus (hair-like structure) which carries adhesins, which facilitate
adhesion to host cell surfaces and receptors.

Invasion
●​ The glycocalyx is a glycoprotein and glycolipid covering that surrounds the bacterium’s
cell membrane.
●​ This protects the bacterium from phagocytes and allows it to attach to host cells.
●​ Induce phagocytosis by expressing surface protein that binds to surface receptors of
host cell → forms vacuole and is engulfed

Replication
●​ Replicate in vacuole
 ●​ Replicate in cytosol

Adaptations of viruses

Adhesion
●​ A peplomer is a glycoprotein spike on a virus capsid (i.e. a surface protein).
●​ These bind only to certain receptors on the host cell, making them essential for host
specificity and thus viral infectivity.

Invasion
●​ Viral particles undergo endocytosis -
movement into the cell.
●​ Enveloped viruses are enclosed within an
endosome formed from the host cell
membrane as they move into the cell.
●​ Harder for host immune system to identify as it conceals its own antigens with the host
cell membrane
●​ Non-enveloped viruses form a pore in the membrane, through which they deliver their
viral genome.
●​ Also enters by direct penetration, fusion with cell membrane

Adaptations of fungi

Adhesion
●​ Adhesion is assisted by the cell wall or the capsule.

Invasion
●​ Thermotolerance: heat shock proteins are manufactured to facilitate the cell’s survival in
body temperatures (which are higher than air temperatures).

Adaptations of macroparasites

Adhesion / invasion
●​ Hookworms
●​ Deep teeth anchor the hookworm firmly to the intestinal epithelium.
●​ Ticks
●​ Specialised mouthparts are inserted into the host’s skin. These secrete
biologically active molecules which prevent the host from initiating an
inflammatory response.

Transmission of disease
Methods of Transmission
●​ Contact transmission
○​ Airborne droplets
○​ Sexual contact
○​ Direct contact
●​ Vehicle transmission
○​ Food and waterborne
○​ Carried in blood
●​ Vector transmission (may have more than one: intermediate host)
○​ Arthropod borne
○​ Fleas
○​ Rodents
○​ Mosquitoes
○​ Ticks
○​ Fruit bat
○​ Foxes

Comparison of adaptations to facilitate transmission between hosts

Complex (indirect) life cycle

●​ More than one host
○​ Primary or final host: pathogen reproduces sexualally
○​ Secondary or intermediate host: reproduces asexually
●​ Examples
○​ Yersina pestis, causes bubonic plague blocks digestive tract of flea, vomits up
bacteria from foregut in a bite to unblock digestive tract
●​ Direct life cycle: transmitted to new host without vector or intermediate species

Attachment structures
●​ Bacteria adhesions: protein structures that helps them bind to the surface of potential
host cell
○​ Helicobacter pylori, cause stomach ulcers
○​ Produce adhesions to attach to stomach epithelium
○​ Cytotoxins create ulcers by destroying epithelial cells
●​ Types
○​ Fimbriae (thinner, shorter, less rigid and more numerous, specialised for
attachment
○​ Pili: involved in attachment and gene transfer

Phagocytosis and endocytosis

●​ Intracellular pathogens (inc viruses) need to enter host cell for growth and reproduction,
avoid contact with antibodies, phagocytes
●​ Trigger endocytosis by binding to membrane receptors, enclosed invisible taken into cell
 ○​ Eg. Influenza A binds with host surface receptors and adenoviruses that cause
cold, etc
●​ Taken in endosome, proteins break down endosomal membrane so virus and enter
cytosol to move into nucleus

Resistant Structures
●​ Help exist outside host
●​ Endospores
○​ Resistant asexual spore that develops inside bacterial cell
○​ Eg bacillus anthracis which causes anthrax
●​ Virion: complete infective form of the virus
○​ Capsid (protein coat)
○​ Genome inside capsid, RNA or DNA
○​ Virulence depends on adaptive features (pH, temperature, humidity)
●​ Viral envelopes
○​ Help virus avoid host immune system
○​ Often less virulent
○​ More sensitive to heat, pH

Transmission Adaptations to facilitate transmission Examples of

route pathogens

Airborne on dust ●​ Able to remain suspended in air for long periods Influenza
and respiratory ●​ Resists drying out
secretions (eg. ●​ Causes sneezing and coughing → new host
water droplets) ●​ Resist wide range of O2 concentrations

Waterborne ●​ Able to colonise in water Legionella,

●​ Modified outer surface structures (fimbria, flagella) allow motility vibrio, giardia,
●​ Marine borne organisms are halotolerant (tolerate high salinity) campylobacter
●​ Not easily destroyed by boiling spp.

Vector borne ●​ Poorly understood Malaria, zika

●​ Special surface proteins that allow attachment to vector tissues
●​ Life cycle of pathogen is synced with feeding habits of host

Faeco-oral ●​ Varied environments E. coli,

●​ Induction of vomiting and diarrhoea increases likelihood of salmonella
transmission
●​ Antimicrobial resistance genes

Epidemics
●​ Sudden outbreak of an infectious disease that spreads rapidly through the population,
affecting a large number of individuals
●​ Populations become susceptible to epidemics when
 ○​ There is no immunity
○​ Pathogen is virulent
○​ Easy means of transmission
○​ Lowered resistance to infection (eg. winter)
●​ Flu epidemics are the most common type of epidemic and occur when the virus mutates
to form a new strain
●​ Sars
○​ 2002-3
○​ 8000 Confirmed cases with almost 800 deaths (10% fatality)
○​ China and Hong Kong
○​ Droplet transmission (eg. nasal secretions from sneezing)

Pandemics
●​ An infectious disease occurring over a large geographical area, usually worldwide
●​ Only five diseases have caused pandemics
○​ Bubonic plague (black death)
○​ Cholera
○​ Spanish Flu
○​ AIDS
■​ Global pandemic caused by human immunodeficiency virus
■​ Most affected by is sub-Saharan Africa
■​ Transmitted from sexual contact, exposure to infected body fluids or
breastfeeding
○​ COVID 19

Case study - Cholera

●​ 1826 - 1837
●​ Bacterial infection (Vibrio cholerae) of the small intestine caused by contaminated food
or water
●​ Symptoms vary in severity and include diarrhea, vomiting and muscle cramps severe
dehydration and potential deaths
●​ Reached India across western Asia to Europe, Great britain, Americas, China, Japan
●​ Many million over the decade
●​ Poor slums worst hit
●​ Science invented that helps future outbreaks
○​ 1832 saline drip invented by Dr Thomas Latta
○​ Replaces fluid lost by cholera patients
○​ Still used today
●​ Microbe identified in 1854 by Fillio Pacini
●​ 1849 John Snow, interviewed London families on water sources → correlation, published
findings
○​ Controversial
○​ 1866, NYC disinfected houses → accepted
○​ Fathers of modern epidemiology
 ○​ Changes in water and waste systems in london and round world

Design and conduct a practical investigation relating to the microbial testing of water or food
samples

Method
1.​ Swab benchtop with alcohol.
2.​ Hold an inoculation loop in the flame of a Bunsen burner until it glows red.
3.​ Unscrew the lid of the container of the water sample.
4.​ Put the loop into the bottle and pick up a film of water. Keep the loop in for a few seconds
to ensure live cells are picked up.
5.​ Lift off the cover of the agar plate just enough to put the loop in it. Treat a control plate in
the same manner (but without water).
6.​ Smear the plate with the loop and replace the lid.
7.​ Flame the loop once more to kill any remaining live cells.
8.​ Seal the agar plate and place it in the incubator at 37 °C for three days.

Investigate the work of Robert Koch and Louis Pasteur, to explain the causes and
transmission of infectious diseases

Pasteur’s on microbial contamination

Historical Debate: spontaneous generation vs biogenisis

●​ Commonly believed spontaneous generation that life can arise from non-living matter,
formed by vital force
●​ 1668 Italian Francesco Redi tried to disprove
○​ 6 jars with decaying meat
○​ 3 jars with net no maggots
○​ 3 open jars
○​ Biogenesis
●​ Biogenesis: Living cells can arise only from pre-existing living cells (Rudolf Virchow)

Pasteur’s contribution
●​ Disproved idea of spontaneous generation, establish Cell Theory (all living things come
from cells)
●​ Decay and spoilage of food caused by air-borne microbes, not just contact with air
○​ Pasteurisation: application of high heat
●​ Suggested microorganisms cause food decay, disproving spontaneous generation
●​ Stimulated scientists to look for microbe that were causing diseases
 Pasteur’s Experimental method

Similar to following the experimental method to prove

microorganisms cause food spoilage - particles in air decay,
not air
1.​ Boil meat broth in order to sterilise
2.​ Pour half of broth in each two sterile flasks
3.​ Attach a rubber stopper with a swan-necked tube to
one flask; this prevents microorganisms from entering.
Leave other flask open
4.​ Leave broth in a warm environment for one week then
observe microorganisms growth in each of the flasks
5.​ Repeated to increase reliability.

Koch
●​ Proved bacteria causes anthrax, TB, cholera
●​ Developed agar techniques
●​ Koch’s postulates
○​ Sequence of experimental steps used to prove
that a specific microorganism causes a specific disease, still in use today

The postulates
1.​ The microorganism must be found in abundance in all organisms suffering from the
disease, but not in healthy organisms
2.​ The microorganism must be isolated from a diseased organism and grown in pure
culture
3.​ The cultured microorganism should cause disease when introduced into a healthy
organism
4.​ The same microorganism must be reisolated from the experimentally infected host

Assess the causes and effects of diseases on agricultural production including but no
limited to plant and animal diseases

Two types of plant and animal diseases are of concern in agriculture in Australia
1.​ Endemic diseases: Diseases that are consistently present within the region
2.​ Exotic diseases: introduced diseases

Three factors contribute to the development of infectious disease in organisms of agricultural

importance
1.​ Host factors: Susceptibility to disease, access to pathogen, concurrent disease or poor
nutrition leading to weakened immune response
2.​ Pathogen factors: Pathogen’s availability, ability to transfer between hosts as well as
virulence factors including adhesion and successful establishment
 3.​ Environmental factors: overcrowding and lack of hygiene leading to build up of wastes
which provide a suitable environment for pathogen reservoirs

Animal Disease - Foot and mouth

●​ Acute skin disease of cloven-hoofed animals caused by virus
●​ RNA virus, infection
●​ Often kills young animals
●​ Fluid filled blisters on feet, glands, mouth of animals → ulcers up to 10 days to heal
●​ Lame and unable to walk, stop eating

Cause
●​ Pick up from infected animal or contact with contaminated soil or food
●​ Coxsackie virus
●​ FMD spreads in cool, damp conditions by saliva mucus milk, faeces, wool hair
●​ Increased risk: increased human population mobility, intensive farming, antimicrobial
resistance, loss of genetic diversity due to inbreeding

Treatment
●​ No cure slaughter and rapid burial
●​ Destroyed by heat, sunlight, low humidity, some disinfectants

Risk to Australia
●​ Key beef, lamb and pork export markets being closed
●​ Tourism
●​ Affect on trade, will impose restrictions on FMD infected countries
●​ Small FMD could cost $7.1 billion (6 months), $16 billion (12 months)

Plant Disease - Panama Disease

Cause
●​ Most destructive diseases of banana plants worldwide
●​ Caused by soil-borne fungus fusarium oxysporum
●​ Spread by movement of infected plant material, but can also spread with soil and water
movement or by contaminated equipment, not airborne

Symptoms
●​ Yellowing of the oldest leaves
●​ Infected leaves fall in order from oldest to youngest → skirt of dead leaves
●​ Younger plant will die soon

Management
●​ All bananas are clones → limited genetic variation → susceptible
●​ No chemical effective → preventative measures
○​ Suckers from fields free of disease
 ○​ Burn infected plants, destroy surrounding weeds
○​ Restrict movement of animals and humans
○​ Sterilise farm tools with disinfectant
●​ If not managed, could have huge impact on Aus banana industry, affecting production,
livelihoods and communities
○​ N QLD grows 95% of Aus bananas

7.2 How does a plant or animal respond to infection?

Plant defense responses

Plant defense responses

Passive (constitutive resistance)

●​ Structural (physical)
○​ Thick cuticles, cell walls, small sized stomata
○​ Leaf orientation
■​ Leaves that do not hang vertically do not accumulate water, reducing
likelihood that pathogens with grow on them
○​ Plant surface coating
■​ All external plant surfaces are coated with lipids, which form a protective
layer which physically blocks the entry of pathogenic microorganisms
○​ External defence penetrated: nematodes use sharp mouth parts to get through
cell walls
●​ Chemical
○​ Plants damaged by insects can release volatile chemicals to warn other plants of
the same species

Active defences (inducible resistance)

●​ Active defences - involves more targeted responses by the plant.
●​ Rapid active response
○​ The release of hydrogen peroxide in an oxidative burst can kill microorganisms.
○​ Any defects in the cell wall are reinforced by the aggregation of lignin in the
cytoplasm.
○​ Apoptosis: programmed cell death: A cluster of dead plant cells accumulates
around the pathogen, starving it of nutrients and water.
○​ Antimicrobial compounds are secreted.
●​ Delayed active response
○​ Limits the spread of a pathogen.
○​ Mechanisms include: Production of cork cell to make bark and repair wounds.
○​ The release of lysozyme-like chemicals which have an antimicrobial action.
○​ The release of salicylic acid acts as a signalling agent. This acid has the
capability of acquiring resistance against particular pathogens, decreasing the
severity of subsequent infections.
 Investigate the response of a named Australian plant to a pathogen

Response of a named Australian plant - potato plant

●​ The potato plant ipomoea costata is an Australian plant that is susceptible to late blight,
a fungal infection.
●​ Host: Ipomoea costata (Potato Plant).
●​ Pathogen: Phytophthora Infestans (Fungi).
●​ Disease: Late Blight (or Potato Blight).

Responses
●​ Beta-glucan receptors
○​ Rock morning glory has specific receptors which recognise the beta-glucans on
the cell wall of the fungus.
○​ When these receptors are stimulated, protease is released, which inhibits the
growth of the fungus.
●​ Resistance proteins
○​ Rock Morning glory has specific resistance proteins that are capable of
recognising antigens.
○​ protease protein is produced as a response to inhibit the effectors molecules
produced by the fungi’s hyphae and stop the growth of the pathogen.
○​ This therefore stop the pathogen’s (or the hyphae) invasion to obtain nutrients
from the plant’s cells that are necessary for fungi growth & survival

Host: Tomato Plant

Pathogen:Tomato Spotted Wilt Virus

Disease: Tomato Spotted Wilt

Animal response to pathogens

Nonspecific and specific defense mechanisms summary

Nonspecific defence mechanisms Specific defence mechanism

(INNATE IMMUNITY) (ADAPTIVE IMMUNITY)

1st line of defence 2nd line of defence 3rd line of defence

Physical: Intact skin, mucous, Phagocytic white blood cells Specialised lymphocytes
cilia (B cells and T cells)

Chemical: urine, sweat, saliva, Inflammatory response Antibodies

tears

Fever

Antimicrobial substances

Lymphatic system

The first line of defence - Barriers to entry

Physical barriers

Skin
●​ Skin physically prevents the entry of pathogens
●​ Predominantly made of dead skin cells - dry, thick and tough
●​ Contains biochemical defence agents (eg oily secretions which inhibit bacterial growth)
●​ Natural microflora on the skin inhibits the growth of the pathogenic bacteria
○​ Antibiotics kill healthy microflora leading to invasion by nasties eg thrush

Cilia

●​ Cilia are tiny hairlike structures which line the trachea

●​ Push pathogens and foreign particles up the windpipe by a waving acting, so they can
be expelled by expectoration or sternutation
●​ Beat like oars with the trapped pathogens
●​ Lined in the upper respiratory system

Mucous membranes
●​ Mucous membranes line the inner respiratory digestive surfaces
●​ They release protective fluids to wash away pathogens (mucus)

Chemical

Urine
 ●​ Micturition - flushing of sterile urine down the urethra - removes pathogens from the
urethra

Sweat
●​ Sweat is an oily material which waterproofs and lubricates the skin
●​ It is acidic, inhibiting the growth of microbes

Saliva
●​ Saliva contains antimicrobial substances which inhibit the growth of microbes in the
buccal cavity.
●​ This antimicrobial action works in conjunction with the physical flushing action of saliva.

Tears
●​ Tears also contain antimicrobial substances, which are distributed evenly over the
surface of the eye, inhibiting microbial growth.

Acid
●​ The stomach is filled with gastric (hydrochloric) acid, whose extremely acidic nature
discourages the survival of microbes.
●​ Vagina has acidic mantly inhibiting growth of fungi and bacteria

The second line of defence (Non-specific/innate immune response)

Antigen
●​ Substance that triggers immune response

Substances released
●​ If host cell detects pathogen apoptosis (controlled cell death) then inflammation
stimulated

Name Description Function

Cytokines General proteins (interferons, Regulate function of lymphocytes and other cells in
interleukin, growth factors) immune system

Interferons Protein activator Activate antiviral genes (Interferon Stimulated

Genes) in infected and neighbouring cells, that
restrict viral reproduction

Interleukin Released by macrophage Cause hypothalamus to release prostaglandins to

induce fever

Chemokines Secreted by cells near infection Directs movement of phagocytes towards wound
(opposite pressure gradient)
 The inflammatory response
●​ Inflammation occurs when blood vessels around the infected area are dilated and
supplied with extra blood.
●​ Swelling, heat, pain.

Substance Made by Stored in Causes

Heparin Liver, mast cells, basophils Cytoplasmic granules Prevents blood clotting,
maintains blood supply

Histamine Mast cells, basophils Cytoplasmic granules Vasodilation, increased vascular

permeability, itching

Serotonin Platelets, mast cells, basophils Cytoplasmic granules Vasoconstriction, increased

vascular permeability

Prostaglandins Cell membranes in nearly all cells Not stored Fever, pain, dilation or
constriction

The process of inflammation

 ●​ Microbial pathogens (e.g. bacteria) enter the skin through a cut or abrasion
●​ Damaged cells and nearby mast cells release histamines and prostaglandins to attract
phagocytes to the infection
●​ The histamine causes the blood vessels to dilate and the capillaries to open pores in
their walls, letting the phagocytes through to the tissues to fight the infection
●​ After a few days, an abscess forms, filled with pus (dead white blood cells).

Phagocytosis
●​ White blood cells - macrophages and neutrophils - can engage in the process of
phagocytosis, where they completely engulf and digest pathogens.

The process of phagocytosis

●​ Phagocyte detects chemicals released by foreign intruder
●​ Moves up concentration gradient towards intruder
●​ Adheres to foreign cell, engulfs in vacuole by infolding of cell membrane
●​ Lysosomes (organelles digestive enzymes) fuse and digest the vacuole
●​ Displays some of the pathogen’s antigens on its surface. (Antigens are protein markers
which induce an immune response; see 7.3)
●​ This communicates the type of pathogen to other immune system cells, and is therefore
the link between the second (non-specific) and third (specific) lines of defence.

Pus
●​ Pus is a waste product composed of dead pathogens and phagocytes.

Formation of a cyst enclosing the pathogen

●​ White blood cells surround the pathogen so it is enclosed in a cyst.
●​ The white blood cells involved then die, so the pathogen is deprived of nutrients and
thus dies.

Fever
●​ A fever occurs when the body temperature is above 37 °C
●​ Fevers are usually indicative of bacterial or viral infection.

Benefits of fever
●​ Intensifies the production of interferons (proteins which inhibit viral replication)
●​ Increases the production of T cells
●​ Speeds up metabolic reactions (e.g. tissue repair)
●​ Increases heart rate so that blood cells are delivered to sites of infection more quickly.

The febrile process

1.​ The individual is infected by a pathogen or toxin
2.​ Macrophages respond - they destroy the pathogenic microorganisms and release
Endotoxins.
 The lymphatic system
●​ System of vessels and lymph nodes that returns protein and intercellular fluid to the
circulatory system
●​ Filters cell debris
●​ Produces white blood cells
●​ Lymph: Colourless fluid in the lymphatic system

Lymph nodes
●​ Filters along lymphatic vessels, remove microbes, foreign particles, tissue debris
Destruction of pathogens occurs mainly at the lymph nodes.
●​ The lymph nodes becoming hard and swollen is a sign that lymph cells are reproducing
rapidly to fight infection​

Complements
●​ Group of 20+ proteins that assist other defence
●​ Enhance phagocytosis
●​ Cause cell lysis (cell membrane disrupted, water and ions enter, intensifies inflammation)

Organ transplants
●​ Immune system will identify the organ as foreign body (antigen)
●​ Stimulate non-specific response such as inflammation and phagocytosis
●​ Specific response of B and T lymphocytes
●​ Tissue rejection → need for immunosuppressive drugs

7.3 Immunity

Inquiry question: How does the human immune system respond to exposure to a
pathogen?

Investigate and model the innate and adaptive immune systems in the human body

The anatomy of the immune system

 ●​ Immune cells develop in the bone marrow and thymus
●​ Immune responses occur in the spleen, lymph nodes, and
lymphatic vessels

The third line of defence (the specific response) - an overview

Antigens
●​ All cells have surface markers.
●​ Body can recognise as self or non-self.
●​ Antigens are surface protein markers which induce an immune
response.
●​ Third line of defence target marked cells with
○​ The humoral immune system
○​ The cell-mediated immune system.

Lymphocytes
●​ Specific immune responses to specific, identified pathogens.
●​ There are two types:
○​ B-cells, made in bone, produce antibodies (humoral
immunity)
○​ T-cells, made in thymus destroy infected cells
(cell-mediated immunity).

Production of lymphocytes
●​ Pluripotent stem cells are produced in the bone marrow.
●​ Develop into immature lymphocytes.
○​ Remain in the bone marrow, and specialise into B-cells
○​ Transported to the thymus via the bloodstream, where they specialise into
T-cells.

Humoral immunity (B-cell immunity, fights EXTRACELLULAR infections)

1.​ B cell activated by matching free antigen
2.​ Antigen presentation: binds with MHC-II molecule on B cell
3.​ Helper T-cell binds to MHC antigen complex via its T-cell receptor
4.​ B-cell releases interleukin-1 (a cytokine), activating the TH cell
5.​ Activated TH cell produces interleukin-2
6.​ Binds to MHC-antigen complex on B-cells, causes them to multiply, creating plasma cells
a.​ Some memory B-cells
 b.​ Long lived, rapidly produce antibodies if same pathogen in body again
7.​ Plasma cells are B-cells produce specific antibodies
8.​ Antibodies combine with antigens at least 2 binding sites
a.​ Enhances phagocytosis
i.​ Pathogens with antigens to lump together, easy recognition and
destruction by macrophages.
ii.​ Or Agglutination of antigen bearing particles
iii.​ Precipitation of soluble antigens
b.​ Cell Lysis
i.​ Complement fixation (activation of complement) → Lesion
Cell-mediated immunity (T-cell immunity, fights INTRACELLULAR infections)
●​ Type of lymphocyte, provides cellular immunity by destroying infected cells
●​ Has antigen receptors: recognise specific antigens, major histocompatibility proteins on
the surface of cells

Helper T-cells (TH cells)

●​ Release cytokines that promote the humoral response
●​ Activate macrophages
●​ Induce formation of cytotoxic T-cells
●​ HIV infects helper T cells

Cytotoxic T-cells (TC cells)

●​ Kill damaged, infected, or cancerous cells
●​ Binding to the MHC-I complexes on the infected cell with their T-cell receptors.
●​ Release perforin, perforates the cell membrane of the target cell, causing lysis (ions and
water enter, cell explodes) → cell death

Memory T-cells (TM cells)

●​ Reactivate quickly in response to subsequent presentations of the same antigen.
●​ (Difference between TM and BM cells: TM trigger TC, BM trigger antibodies)

Suppressor T-cells (Ts cells)

●​ Stop the immune response when the antigen is destroyed.

Action of cytotoxic T-cells

●​ Cytotoxic T-cells recognise infected cells by the antigens displayed on MHC-I
complexes.
●​ Contacts infected cell, releases perforin, granzymes and granulysin, which cause lysis,
apoptosis and DNA fragmentation.
●​ Can also release interferon gamma in response to viral infections: blocks intracellular
viral replication without lysing the cell itself.
○​ Lysing cell would release the viruses into the intercellular fluid, aggravating the
infection.

Interactions between B and T lymphocytes

●​ Helper T cells stimulate B cells and T cells to clone via the release of cytokines such as
interleukin-1.
●​ Systems to allow B and T cells to identify that they both belong to the body and not to
attack each other include the presence of major histocompatibility proteins.
●​ MHC proteins on the surface of cells allow for the identification of “self” versus foreign
cells.
 Process of T-cell immunity
1.​ Foreign material is engulfed by macrophages (2nd line), which then display the antigen
attached to their MHC-II molecules.
2.​ The antigen-presenting macrophages move to the lymph nodes, where they are
inspected by helper T cells that have the T cell receptor that corresponds to the antigen
being presented.
3.​ These helper T cells then activate the cloning of millions of cytotoxic T cells and memory
T cells that are specific for this antigen
4.​ The cytotoxic T cells leave the lymph nodes and migrate to the site of the infection,
where their antigen receptors bind with the antigen displayed on the infected cell.
5.​ These T cells then release chemicals that destroy the cell and any pathogens within it.
6.​ These chemicals also increase the inflammation and attract more macrophages, which
carry out phagocytosis to help destroy the pathogens and clear up any debris
7.​ Some of the cytotoxic T cells produce cytokine interferon, which protects the healthy
cells around an infected cell from viral invasion
8.​ Once the infection has been defeated, the suppressor T cells release other chemicals to
stop the production and action of the cytotoxic T cells.
9.​ The memory T cells that are produced at the time and are specific to that particular
antigen remain in the body, in the lymph nodes. On re-exposure to the same
antigen-containing pathogen, they cause the rapid production of more of the same
cytotoxic T cells. This prevents the body from developing the symptoms of the disease
again.

OR

1.​ Antigen presenting (infected cell) presents an antigen fragment on Class I MHC to TC
2.​ TC

Diagram of both
 Explain how the immune system responds after primary exposure to a pathogen including
innate and acquired immunity

Naturally Acquired Immunity

Passive
●​ Antibodies passed from mother to fetus via placenta during pregnancy or through milk
●​ Infant does not produce antibodies
 Active
●​ Antigens enter body → immune response → acquired immunity
●​ Produced specialised lymphocytes and antibodies
●​ attached to pathogenic microorganisms in the normal manner
●​ This prompts the body to produce specialised B and T cells, as well as antibodies.

Artificially acquired immunity

Passive
●​ Preformed antibodies introduced into body by injection
●​ Body does not produce antibodies
●​ Eg. anti-venom

Active
●​ Active → the body makes the antibodies
●​ Weak/dead introduced in vaccines
●​ Produces specialised lymphocytes and antibodies

Patterns of antibody levels during clinical infection

Primary response
●​ Delay whilst macrophage is looking for the correct TH cell is being found to present
antigen to
●​ Gradual increase in antibody levels when TH cell activated
○​ Secreted cytokine (interleukin-2)
○​ Activates clones of B cells, produce antibodies (peak)
○​ TC cells cloned
○​ Memory T cells produced, remain in the lymph system
 ○​ Some B cells ares plasma cells, some memory cells
●​ Gradual decline of antibodies follows, pathogen has been defeated, no need
●​ But does not go to 0, with memory B cells still present

Secondary response
●​ Antibody response is FASTER and MORE INTENSE to same antigen
○​ Left behind memory B-cells (not T cells because antibodies) have been
●​ Due to existence of memory cells which rapidly produce plasma cells upon an antigen
stimulation
●​ Memory T and B cells respond within hours, rather than days, preventing symptoms
appearing
●​ Higher peak
●​ Vaccines can stimulate same response

After initial exposure to antigen, no antibodies are found in the serum for a few days.

A gradual increase in antibody levels is noted as TH cells are activated:

The TH cells secrete the cytokine interleukin-2, which activate cloning of plasma B-cells (which
produce large amounts of antibodies), as well as cloning of TC cells, which attack infected cells
directly.

TM and BM cells are produced during the initial exposure, which remain in the lymph system. If
the body encounters an infection bearing the same antigens again, the memory cells will trigger
a much stronger and faster immune response.
After the initial infection has been fought off, a decline in antibody count follows.

Subsequent infections
Subsequent exposure to the same antigen results in a stronger and faster immune response,
due to the memory cells, which reappear within hours of infection (as opposed to days).
Vaccines also stimulate this response (as they pre-expose the host to the antigens).

7.4 Prevention, treatment and control

Inquiry question: How can the spread of infectious diseases be controlled?

Investigate and analyses the wide range of interrelated factors involved in limiting local,
regional and global spread of a named infectious disease

Multi drug resistance

●​ Antibiotics losing power → renewed virulence (re-emerging)

Emerging infection disease

●​ No previous history in human population
 Re-emerging
●​ Previously known, increasing incidence

SARS: Severe Acute Respiratory Syndrome

●​ 2002 in china: feces of infected horseshoe bats
●​ Spread through human contact (coughing and sneezing)
●​ Coronavirus
●​ 10% death rate, 50% for 60+ years

Development
●​ Quickly
●​ Health systems were strained
●​ Aided by global air travel

Public Health Measures

●​ Tracing of every possible contact with SARS
●​ Immediate quarantine (enforced with threat of execution in China)
●​ Surveillance systems upgraded
●​ Infection control procedures tightened in hospital

Containment
●​ Mass education campaigns
●​ Frequent fever checks

Malaria
●​ Malaria is an infectious disease caused by a plasmodium, spread by the female
Anopheles mosquito.

Limiting the spread of malaria Local measures (town, city)

●​ Using insecticide-treated bed nets
●​ Installing window screens
●​ Using insect repellents

Regional measures (country, continent)

●​ Applying chemical insecticides directly to the larval habitat
●​ Carrying out source reduction by draining swamps to reduce mosquito breeding habitats

Global measures
●​ Development of rapid, mass-produced diagnostic tests
●​ Mass treatment using antimalarials
●​ Development of a vaccine
●​ Limiting international travel to reduce global spread of disease
 Investigate and assess the effectiveness of pharmaceuticals as treatment strategies for
the control of infectious disease

Factors which limit effectiveness of pharmaceuticals

●​ Cost effectiveness of producing new drugs
●​ Time taken to produce new drugs

Antibiotics
Antibiotics are pharmaceuticals that kill or inhibit growth of bacterial infections

How they work

●​ Inhibiting activities such as cell wall synthesis and protein synthesis.
●​ If cell wall synthesis is inhibited, defective portions of the cell wall cannot be repaired,
making the bacterium susceptible to lysis.
●​ If protein synthesis is inhibited, the bacterium cannot manufacture the proteins and
enzymes required to carry out metabolism, leading to cell death.

Factors which limit effectiveness

●​ Patients often do not complete courses of prescribed antibiotics, leading to the
proliferation of those bacteria which survived (are resistant to) the antibiotic treatment.
○​ VERA
○​ Variation exists
○​ Environmental selective pressure give variation advantage
○​ Reproduction
○​ Adaptions more prevalent
●​ Antibiotics are used excessively in livestock feed. The excess drains off into waterways
and the surrounding environment, resulting in the development of antibiotic resistance in
the surrounding ecosystem.
●​ Unregulated access in developing countries contributes to the development of antibiotic
resistance.

Investigate and evaluate environmental management and quarantine methods used to

control an epidemic or pandemic

Australian Health Management Plan for Pandemic Influenza

●​ The Australian Health Management Plan for Pandemic Influenza (AHMPPI) is a planned
official response to a pandemic outbreak of influenza.

Management and quarantine methods

●​ Locking down borders to delay entry of virus into Australia
●​ Containing known cases through quarantine and isolation
●​ Health campaigns promoting public hygiene
●​ Large-scale public vaccination programs
 Evaluation
Preparedness Public health leadership Media management

Plan is in place and ready to Supply chains created for Public fear controlled by
be implemented medications and vaccines limited release of information

Surveillance and mandatory Large scale analysis of

reporting of known cases epidemiological data allows
reduce transmission rates trends in infection rates to be
forecasted

Antivirals
●​ Antivirals are pharmaceuticals used to treat viral infections.
●​ They work by inhibiting the replication of the virus.
●​ Factors which limit effectiveness
●​ Antiviral drugs often also harm the host cells while inhibiting viral replication.
●​ Antiviral therapies are available only for a small number of viral infections (e.g. hepatitis
B, HIV, herpes).
●​ Viruses mutate extremely rapidly, meaning that resistance to antiviral drugs is developed
rapidly.

Smallpox vaccine

●​ One of the deadliest diseases known to humans

●​ (2016) the only human disease to have been eradicated by vaccination
●​ The smallpox vaccine, introduced by Edward Jenner in 1796, was the first successful
vaccine to be developed.
●​ He observed that milkmaids who previously had caught cowpox did not catch smallpox
and showed that inoculated vaccinia protected against inoculated variola virus.
●​ The global eradication effort initially used a strategy of mass vaccination campaigns to
achieve 80% vaccine coverage in each country, and thereafter by case-finding, followed
by ring vaccination of all known and possible contacts to seal off the outbreak from the
rest of the population.

Interpret data relating to the incidence and prevalence of infectious disease in

populations
●​ Type of data: incidence and prevalence of disease: pool of pathogens already in a
population
●​ Mobility of the population: how easy for pathogen to spread
●​ Percentage of the population that is immunised: what proportion of population is
vulnerable
Incidence
●​ Number of new cases occurring during a specified time per population
●​ If expressed as a percent or number per 100/1000, it is also the infection rate
(probability/risk) of contracting disease
●​ Everyone in denominator must be at risk (can become a member of numerator)
●​ If people enter/leave population, denominator must be altered (if someone dies before
time period, must be removed from pool)

𝑛𝑒𝑤 𝑐𝑎𝑠𝑒𝑠 𝑑𝑢𝑟𝑖𝑛𝑔 𝑎 𝑠𝑝𝑒𝑐𝑖𝑓𝑖𝑒𝑑 𝑡𝑖𝑚𝑒

𝑠𝑖𝑧𝑒 𝑜𝑓 𝑝𝑜𝑝𝑢𝑙𝑎𝑡𝑖𝑜𝑛 𝑎𝑡 𝑠𝑡𝑎𝑟𝑡 𝑜𝑓 𝑚𝑜𝑛𝑖𝑡𝑜𝑟𝑖𝑛𝑔 𝑝𝑒𝑟𝑖𝑜𝑑
× 100%

Prevalence
●​ Proportion of population that has the disease at a particular point
●​ Prevalence also depends on length of time taken to cure
●​ Who already has, who just got
●​ Decreases
○​ Death
○​ Cured
●​ Increases
○​ Treatment good but survives with disease
○​ Long disease
○​ Chance of death reduced

𝑎𝑙𝑙 𝑐𝑎𝑠𝑒𝑠 𝑖𝑛 𝑎 𝑝𝑜𝑝𝑢𝑙𝑎𝑡𝑖𝑜𝑛

𝑝𝑜𝑝𝑢𝑙𝑎𝑡𝑖𝑜𝑛
× 100%

Pebbles in a vessel
●​ Incidence: pebbles coming in → infectiousness
●​ Prevalence: pebbles in vessel → disease burden, help plan health services
●​ Deaths/cure goes up, prevalence decreases, no change on incidences
●​ Quick recovery or quick death → prevalence lower