HSC Biology Syllabus Notes
Module 7 / Inquiry Question 1
Overview of Week 9 Inquiry Question – How are diseases transmitted?
Learning Objective #1 – Describe a variety of infectious diseases caused by pathogens, including microorganisms, macro-organisms and non-cellular pathogens, and collect primary and secondary-sourced data and information relating to disease transmission, including:
Classifying different pathogens that cause disease in plants and animals.
Investigating the transmission of a disease during an epidemic.
Design and conduct a practical investigation relating to the microbial testing of water or food samples.
Investigate modes of transmission of infectious diseases, including direct contact, indirect contact and vector transmission.
Learning Objective #2 – Investigate the work of Robert Koch and Louis Pasteur, to explain the causes and transmission of infectious disease, including:
Koch’s postulates
Pasteur’s experiments on microbial contamination
Learning Objective #3 – Assess the causes and effects of diseases on agricultural production, including but not limited to:
Plant diseases
Animal diseases
Learning Objective #4 – Compare the adaptations of different pathogens that facilitate their entry into and transmission between hosts
Overview of Week 9 Inquiry Question
Welcome to Week 9 of your HSC Biology Syllabus Notes!
In this week, we will introduce and examine the topic of infectious diseases.
First, we will explore the role and different types of pathogens responsible for causing a range of diseases.
Once we have done that, we will examine how infectious disease can spread via different pathways.
Next, we will examine how an infectious disease can lead to an epidemic!
Following this, we go over a practical that you will do at school to test the presence of microbes in water and food samples.
After that, we will have a look back in history to explore the work performed by Robert Koch and Louis Pasteur on infectious Diseases.
Following that, we will have explore few examples of plant and animal diseases that are affecting the modern agricultural industry.
Finally, to wrap up this week’s notes we will explore the adaptations of different pathogens that allow them to enter, infect host organisms and spread to other unaffected organisms.
Learning Objective #1 - Describe a variety of infectious diseases caused by pathogens and non-cellular pathogens. Also, collect data relating to disease transmission
Before we can explore the range of infectious disease that is caused by pathogens, it is important to understand introduce the definitions of infectious disease, disease and pathogens.
Pathogen – An infectious agent that is capable causing a disease in a host.
Host – Any organism that carries another organism (e.g. bacteria) or agent (e.g. virus).
Infectious Disease – A disease that is caused by a pathogen or infectious agent and the disease can be transmitted from one (affected) organism to another.
While we are at it, we might as well introduce the definition of non-infectious disease as we will be examining it the upcoming weeks.
Non-Infectious Disease – A disease that is NOT caused by a pathogen and is unable to be passed from one organism to another.
Exception: Inherited Disease is often classified as a non-infectious disease as it can be passed from one organism to another.
Now, what is the definition of disease and health?
Disease – An abnormal structural or physiological condition that harms the living organism and lowering its productivity or usefulness.
Notice that this is very broad. As per definition, the fracturing of a bone resulting not being able to work may be classified as a disease according to the above definition.
Compared to definition of disease, the world health organisation (WHO) defines Health as “a state of complete physical, mental and social wellbeing and not merely the absence of disease or infirmity”.
Viruses
This is a class of non-cellular pathogen.
Description of Virus:
Virus is classified as a non-cellular pathogen as they have living and non-living features. They are not made up of cells but rather they have a protein coat containing genetic information in the form of DNA or RNA.
This means that they are able to pass on their genetic information via DNA/RNA replication and produce more virus via protein synthesis.
It is important to note that a virus cannot reproduce by itself but must rely on a host cell for replication. This is because it does not have ribosomes and uses the host cell’s organelles and reproductive mechanisms to replicate itself.
The protein coat allows the pathogen have surface proteins that enable it to bind to surface receptor proteins on the host cell via complementary binding. It can then enter the cell via endocytosis which we will discuss in detail later.
There are many non-endocytoic pathways which we will discuss later.
Antibiotics are used to destroy cells or disrupt cell metabolism and so are effective against bacteria. However, Viruses do not have cells or perform metabolic activities and thus antibiotics are ineffective against them.
Vaccines are often used to defend against viral diseases by triggering a ‘false-alarm’ immune response that will protect against virus when there is a real attack. We will formally introduce and explore how vaccines work in later weeks.
Name of Virus: Influenza Type A Virus
Name of disease: Influenza A
Symptom:
Sore throat
Fever
Headache
Fatigue
Mode of Transmission:
Air transmission via water droplets from sneezing or coughing.
Inhalation or oral ingestion after unknowingly touching the virus (e.g. park bench).
Bacteria
This is a class of cellular pathogen.
Description of Bacteria:
Bacteria are unicellular, microscopic organisms without membrane-bound organelles. This means that they are prokaryotes and do not have cell membrane.
That being said, they do have a cell wall that may be surrounded by a capsule (jelly-polysaccharide layer).
Bacteria have a circular thread of double helix DNA which is in the form of a single, large chromosome in cytoplasm. They also have plasmids which are circular DNA molecules.
They undergo asexual reproduction via the binary fission process.
Bacteria basically exist ‘everywhere’ that we go and many are actually beneficial to us.
The harmful bacteria cause disease by asexually reproducing inside host organism and secrete toxins that are harm the host organism’s cells, tissues or organs.
We can kill bacteria using antibiotics.
They are often classified into according to their shape. The common groups are spherical, rod, spiral, comma or oval shape.
Some bacteria have a ‘tail’ called flagellum that allows them to move in water.
Name of Bacteria: Mycobacterium Tuberculosis
Name of disease: Tuberculosis
Symptoms:
Coughing (including coughing blood)
Chest pain
Fever
Chills
Mode of Transmission:
Air transmission via water droplet (released due to coughing or sneezing)
Protozoans
This is a class of cellular pathogen.
Description of Protozoan:
Protozoan are unicellular, eukaryotic organisms.
They means that they have cell membranes although they don’t have cell wall.
Similar to bacteria, they asexually reproduce via binary fission and have DNA as their genetic material.
They are heterotrophic organisms, which means they cannot photosynthesis to make their own food.
Many protozoans are live in water and they are mobile in water due to the presence of a ‘tail’ called flagellum. Others have hair-like projections surrounding the pathogen called Cilia that allow the pathogen to move in water.
Name of Protozoan: Plasmodium
Name of disease: Malaria
Symptoms:
High fever
Vomiting
Chills
Abundant sweating
Mode of Transmission:
Vector Transmission (i.e. Mosquito bite injecting pathogen into host organism)
Fungi
This is a class of cellular pathogen.
Description of Fungi:
Although fungi can be unicellular (e.g. yeast) or multicellular (e.g. mushroom), they are all eukaryotes. This means that they have membrane-bound organelles. They also have a rigid cell wall made from chitin.
Unlike bacteria and protozoan, they are not motile (non-mobile). They reproduce via spores and spores rely on wind for transportation which germinates upon landing on a surface in a favourable environment such as presence of moisture and preferably cool temperatures.
Fungi can either be living on dead tissue (known as saprophyte) or be parasites (thrive on living tissue).
Name of Fungi: Microsporum
Name of disease: Athlete’s foot or Tinea
Symptoms:
Scaly, dry skin
Itching and burning between toes or bottom of foot.
Peeling of upper layer of foot’s skin.
Mode of Transmission:
Direct contact with fungus (e.g. infected person can transfer fungus to an object which is a healthy host makes contact. Another way can be through the direct contact between infected and unaffected organisms)
Macroparasites
This is a class of cellular pathogen.
Description of Macroparasite:
This type of eukaryotic pathogen is multicellular and is visible to the human eye. They can be divided into two groups being endoparasites and ectoparasites.
Endoparasites lives inside the host organism’s body and obtains food and ectoparasites lives outside the host’s body (e.g. consuming the host’s blood and injecting neurotoxins)
Ectoparasites can also have the role as vectors by carrying other pathogens and infecting other healthy hosts.
Name of Macroparasite: Tapeworm
Name of diseases: Tapeworm Infestation
Symptoms:
Diarrhoea
Vomiting
Weight Loss
Stomach Pain
Vitamin and mineral deficiencies
Mode of Transmission:
Faeces-Oral Transmission. For example, an infected organism can secrete tapeworm eggs which can contaminate food and water. An individual will be infected upon consuming the tapeworm larvae.
Prions
This is a class of non-cellular pathogen.
Description of Prions:
Prions are classified as non-cellular pathogen as they do not contain any DNA or RNA. Normally, the host organism produces normal protein (PrPC) that are responsible for producing neurone synapses are specified by the Prnp gene.
We will learn about neurone synapses in later weeks.
If an organism inherited mutated Prnp gene, an abnormal protein called PrPSc (i.e. Prion) can be specified resulting the destabilisation and degradation of neurone synapses. This results in cell death in brain and cause a range of diseases such as Scrapie, Mad-Cow Disease, Kuru, etc.
There are naturally occurring cells that move around the body that removes dead cells. So, as a result, the dead nerve cells in the brain (due to Prion caused diseases) are removed resulting in ‘holes’ in the brain.
The mutated protein (Prion) is resistant to high temperature, high pressure, digestion by lysosome, UV radiation and toxic chemicals. Hence, they are not readily denatured even under abnormal conditions.
It is important that both the amino acid sequence for the normally folded protein (PrPC) and the misfolded protein (PrPSc or Prion) are the same.
That being said, their three dimensional protein structure are different.
The PrPSc protein activates enzymes that are able to modify the PrPC protein’s structure, resulting the conversion of PrPC proteins into prions (long fibre structures).
Example of Prion: Prion protein PrPSc
Example of Disease: Creutzfeldt-Jakob Disease
Symptoms of Disease:
Memory Loss
Impaired thinking
Difficulty walking
Difficult speaking
Blurred vision
Depression
Random, involuntary twitches around different parts of body.
Mode of Transmission:
Indirect contact transmission such as through contaminated surgical instruments or
Direct contact by eating beef containing the infectious protein.
SIDE NOTE: Food poisoning would be considered a form of indirect contact transmission if the food was contaminated by a host (rather than directly by pathogen), where the host transferred the pathogen to the food. Then, an unaffected species eats the infected food.
However, if the food was contaminated directly by a pathogen and an unaffected species eats it, then food poisoning in this case would be considered direct contact transmission of disease.
Investigating the transmission of a disease during an epidemic
The following factors must be present in order for a disease to occur:
Factor 1: A pathogen.
Factor 2: A susceptible host.
Factor 3: A favourable environment for pathogen to reproduce or replicate.
4th Factor (for transmission between affected and unaffected individuals): In order to transmit the disease from one affected organism to another, a mode of transmission of the pathogen is required. Sometimes, an organism acting as vector must be present to carry the pathogen (e.g. virus) from an affected host to an unaffected host. Therefore, in such scenario, the vector will be acting as the mode of transmission of pathogen.
An epidemic is a situation where there is a change in the disease intensity (or occurrence) in a host population across a period of time.
NOTE: Epidemic does not directly refer to the amount of organisms affected by a particular disease being a high level.
We will study epidemics in greater detail when we have a look at epidemiology (study of the spread resulting in a change in disease intensity) in Module 8 but in this learning objective, we will examine one epidemic event that occurred in Australia.
This change in disease intensity (or number of occurrence) can be attributed to one of the above four factors that have mentioned being altered.
An example of an epidemic is the Equine Influenza or Horse Flu outbreak that occurred in Australia in 2007.
Pathogen causing the Equine Influenza: Equine Influenza Virus (a strain of Influenza Type A Virus)
Transmission of the pathogen:
The virus can spread between horses via nasal discharges that are produced
When infected horses cough, they secrete nasal discharges containing the virus which can be inhaled by unaffected horses.
Farm equipments such as tack and water feeding buckets contaminated by affected horses can also carry and transfer virus can be transferred between affected and unaffected horses.
Humans can also carry the virus on skin, hair, clothing or shoes and transfer the virus to horses.
When the horse inhales the virus, the pathogen replicates in the upper respiratory tract. When the numbers of pathogen is great enough, the virus will breakthrough the cells and causing further nasal discharges by the horse. This spreads the virus to other surrounding horses or to farming equipment.
Method for the elimination of the Equine Influenza Virus (and thus disease) in Australia:
NOTE: The term elimination in the field of infectious disease refers to reducing the incidence of the disease at a specific region to zero.
To eliminate the virus, the government put a halt to all movements of horse between locations and performed quarantine operations to isolate affected and unaffected horses.
During quarantine, the horses were resting and given anti-inflammatory drugs to fight the virus. There is currently no antiviral drugs available to combat the virus if the affected horse was no vaccinated prior to contracting the disease (or being infected by the virus)
Preventive measures for future:
The horses should be vaccinated to kill and be protected from contracting the disease. Since viruses mutate regularly, it is important to keep the horses up-to-update with their vaccinations. In order for this happen, there must continuous monitoring of the strain of virus that is responsible for causing the Equine Influenza Disease.
Another preventive measure includes avoiding sharing equipment (e.g. water buckets and grooming aids) between horses. This therefore hinders the mode of transmission for the virus between affected and unaffected hosts.
Control measures for future:
Affected horses should be isolated from unaffected horses to minimise the transmission of disease.
New horses should be quarantined for 14 days before grouping the new horses with existing unaffected horses.
We will examine the difference between preventive and control measures when we explore Influenza A soon.
Design and conduct a practical investigation relating to the microbial testing of water OR food samples
Equipment:
Food sample (e.g. bread, yogurt and cheese)
6x Agar plates
1x Incoulating loop
1x Bunsen Burner
Alcohol (e.g. Baby wipes)
3x Test tubes
Pen & Labels
Sticky tape
Procedure:
Step 1: Sterilise table surfaces using alcohol (e.g. baby wipes)
Step 2: Sterilise your inoculating loop by heating it in the flame of bunsen burner. Also, sterilise three test tubes by heating the ‘mouth’ of the test tubes to restrict/minimise pathogens in the air entering the tubes.
Step 3: Transfer small quantities of three different food sample into three test tubes with 2mL of distilled water and gently mash up the food samples.
Step 4: Dip your sterilised inoculating loop into the food sample in one of your test tube and wipe the food gently on the surface of your agar.
Step 5: Put on the agar plate lid and seal the plate using the sticky tape then label the food type on the lid.
Step 6: Heat your inoculating loop again and repeat Step 4 and Step 5 for your two other types food samples in Test Tubes 2 and 3.
Step 7: Leave 3 sealed agar plates as your control.
Step 8: Observe the number of microbial colonies that are formed in each agar plate and record observations.
Safety First!
Wear gloves to avoid being infection by bacteria.
When you have sealed the agar plate, do not open it again.
Take care of using the bunsen burner and hot inoculating loop.
Wash your hands thoroughly using water and hand-wash solution before leaving the laboratory.
Investigate modes of transmission infectious diseases, including direct contact, indirect contact and vector transmission
Example of Disease transmitted via Direct and Indirect Contact: Influenza A
Pathogen causing Influenza A:
Influenza Type A Virus (a Virus)
Transmission of Influenza A or Pathogen:
Direct Contact: When an infected person sneezes or coughs, water droplets containing the influenza type A virus is trapped which can be enter the mouth or be inhaled through the nose a healthy organism nearby.
Indirect Contact: The infected person’s hands can be contaminated with water droplets (containing the virus) during sneezing or coughing. The infected person then may touch an object (e.g. handrail). If a healthy, uninfected person touches the handrail at the same spot and places his or her hand on their nose or mouth (e.g. touching food and eating without washing hand) then the virus can also enter the respiratory tract.
Influenza A Prevention Measures:
The primary measure in preventing infection from Influenza A Virus is through the use of influenza vaccines. As the virus mutates frequently, it is important to stay up-to-update with the latest vaccine to have the greatest protection against the virus. That being said, this is also why the vaccines may not always be effective as the virus mutates frequently.
Some other preventive measures include wearing protective face masks so that you will reduce your chances in inhaling the virus or inhaling water droplets from affected individuals.
You can also stay away from highly populated areas to minimise the obtaining of disease from affected people.
Influenza A Control Measures:
Following international quarantine procedures to stop the transmission of disease from one location to another (e.g. between countries).
Hosting and running programs to educate people at risk of contracting the pathogen to take preventive measures to not be infected by the pathogen such as vaccination.
Isolating infected organisms from the unaffected organisms to reduce the incidence of the disease. This can be ordering affected employees to remain at home and not commute to work.
What is the difference between control and preventive measures?
According to the World Health Organisation, prevention measures include preventing the occurrence of disease as well as stopping its transmission and effects on society & environment when the disease occurred in nature.
Control measures deals with reducing:
The incidence of the disease
The duration of the disease (and thus lowering risk of the disease spreading to healthy people as the number of affected people spreading the disease at a given time decreases)
The financial burden to affected individuals, their families and affected community as a whole.
Therefore, it is clear that control is part of disease prevention after the disease has occurred in nature.
Example of Disease transmitted via Vectors: Malaria
Pathogen causing Malaria:
Plasmodium (a protozoan)
Transmission of Malaria or Pathogen: Vector to Host Transmission
1. Plasmodium first infects Anopheles Mosquito by entering their stomach and transported to the blood and salivary glands.
2. The infected female mosquitoes bites a human to obtain blood necessary for their eggs to mature. During the bite, saliva containing the plasmodium pathogen is injected into the human’s blood. This pathogen is immature known as sporozoite which are carried to the liver whereby they produce merozoites.
3. The Plasmodium merozoites develops and reproduce inside the liver cells where the cells rupture due to amount of merozoites. These pathogen then migrate and invade other red blood cells via the blood. The same cycle occurs where the pathogen reproduce and rupture red blood cells.
4. Some of the pathogens reproduce sexually to produce male and female gametocytes which a second mosquito will uptake when the affected human is bit.
5. The second mosquito’s (vector) stomach produces the medium for the male and female gametocytes to come to form sporozoites.
6. The cycle repeats itself.
Malaria Prevention
Vector (Mosquito) control is the primary way of preventing malaria infection for people at risk of infection. These vector control techniques can be in the form of installing insecticide coated mosquito nets and screens on windows & doors.
Another preventive measure include spraying insecticides in the homes of the people at risk (known as indoor residual spraying).
Indoor residual spraying is effective in prevention mosquitoes rest on walls or roof prior to biting. During this time, the mosquito will come in contact with a strong dose of insecticide.
It is important to note that strains of Anopheles mosquitoes being resistant to insecticides and antimalarial drugs have evolved.
Antimalarial drugs can also be used to prevent risk of being contracting the malaria disease.
Other preventive measures includes:
Adding larvicides and draining existing and potential mosquito larvae breeding sites
Establishing sufficient rainwater draining system to minimise the amount of mosquitoes near houses.
It is important to note that strains of Anopheles mosquitoes being resistant to insecticides and antimalarial drugs have evolved. Therefore, it’s important to develop new drugs that the mosquitoes are not resistant to.
Malaria Control
Host and run educational program to encourage people at risk of contracting malaria (or pathogen) to take prevention measures to not be infected with the disease (e.g. getting bitten by mosquitoes).
EXAMPLE: Informing the wear of long-sleeved clothing and pants to prevent mosquito bites, using mosquito repellants when venturing outdoors, antimalarial drugs, etc.
Following international quarantine procedures to stop the spread of disease from one area to another (e.g. one country to another).
Increasing global awareness of malaria’s negative impact in various parts of the world to gain funding and make antimalarial drugs more accessible to affected individuals. This would minimise the duration of disease in affected people. Many people in third world countries like Nigeria are dying as they cannot afford such drugs and resort to various herb treatment (many of which is ineffective and only finding out that the disease has worsen over time).
Learning Objective #2 - Investigate the work of Robert Koch and Louis Pasteur, to explain the causes and transmission of infectious disease, including:
- Koch's postulate
- Pasteur's experiments on microbial contamination
Koch's Postulates
There are four postulates established by Robert Koch that can be used to verify whether a specific pathogen causes a specific infectious disease.
In order of experimental procedure, these postulates were:
1. The pathogen must be associated or responsible for all causes of the disease.
2. The pathogen must be able to be isolated from the affected host, grown in a pure culture and recorded for its characteristics.
3. When the newly cultured pathogen is inserted into a new, healthy (unaffected) host, it must result in the new healthy host in developing the same disease (e.g. same symptoms)
4. The pathogen must be able to be isolated from the newly affected host and shown to be same pathogen (e.g. same characteristics) that was isolated from the original affected host.
NOTE: These postulates can be applied to both infectious disease developed in fauna and flora.
This is particularly important as the affected organism or host cell may have interact with many other types of pathogens that are not responsible for causing the disease.
Fun Note: The fourth postulate involving the re-isolating the pathogen in the newly affected organism was actually added by a biologist (E.F Smith) years later after Koch’s proposal of the postulates. Either way, we refer all four of the criteria above as the Koch Postulates.
Koch's experimental procedure that led to the development of his Postulates
The postulates were proposed (1880s) after Koch’s success in establishing that pathogen (a bacterium to be specific) by the name TB Bacillus is responsible for the cause of tuberculosis (infectious disease).
Koch was interested in studying Tuberculosis because it was a highly prominently disease during the time. The disease was responsible for causing 1/7 of the people who died during the time. That’s insane!
During the time, scientists observed that when the organs from affected individuals are transplanted or transferred to an unaffected living organism, the unaffected organism would develop tuberculosis.
Based on this information, Koch theorised that the pathogen that caused tuberculosis was a bacterium. He proposed that the bacteria for the disease was present in the affected organs and thus transplants would also transfer the bacteria to the unaffected organism.
That being said, microscope observation performed during the time did not reveal any image of micro-organism present in affected patient’s organs.
To confirm his theory that a bacterium was responsible for the Tuberculosis disease, Koch devised his own staining technique to stain organs that were affected by the disease. As a result, by observing the stained, affected organs under a microscope, he observed rod-shaped microbes.
The same rod-shaped microbes were observed across other affected organs by Tuberculosis.
That being said, Koch knew that there was a problem. The rod-shaped microbes may have been produced as a result of the disease rather than the cause of the Tuberculosis. So, Koch needs to prove that the microbe was indeed the cause rather than a product.
To do this, Koch carefully isolated some of the microbes from the affected organs and grew them in a pure culture environment containing nutrients. As the temperature of the culturing environment must be correct, Koch had to experiment with a range of conditions until he found an appropriate one.
It took over a week for new bacteria to grow and when they are grown and visible to the eye, they were put into separate environment with new nutrients.
The newly cultured bacteria were transferred into four guinea pigs where another two pigs were used as a control (without bacteria injected). It was observed that all of the four guinea pigs that were injected with the microbe developed the same Tuberculosis disease. The two pigs used as a control did not develop the disease. Koch also replicated this experiment on other animals.
After the end, Koch investigated the mucus and saliva obtained from affected humans. He found that the same microbe was present in the mucus of affected individuals which (again) he found can cause the same disease when injected into unaffected organisms.
Pasteur's experiments on microbial contamination
One of the most important results of Pasteur’s experiments on microbial contamination is that it disapproves the theory of Spontaneous Generation.
Spontaneous generation is the concept where living organisms come to life from non-living matter.
Pasteur disapproves the theory of spontaneous generation through the use of a swan-necked flask to show that microbes arose from other microbes rather than from non-living matter.
A meat broth was placed in both flasks and they were boiled to kill all microbes. Both flask containing the same meat broth was allowed to stand for weeks.
The flask with the swan-necked (or “S” shape) did not develop any microbial colonies. Comparatively, the flask without the “S” shape had microbial colonies formed on the surface of broth.
The experimental result support Pasteur’s proposal that microbes or germs did not arise from spontaneous generation.
Prior to investigating the correctness of spontaneous generation, Pasteur worked on problems regarding the spoiling of wine, beer and the souring of milk. He proposed that microbes in the air that got into the wine, beer and milk were responsible for this.
This proposal of his was derived from his comparative observational studies. Pasteur saw that the desired fermentation reaction of grapes to produce alcohol had the presence of small, round yeast (pathogen) microbes.
Contrastingly, in undesirable fermentation of grapes which produces lactic-acid in wine, it was observed that thread-shaped lactic acid bacteria were present.
From this, Pasteur stated that both there are two types fermentation reaction in the production wine and beer, each required the presence of microbes. Pasteur said that was the presence of the presence of lactic acid bacteria microbes that contributed to the spoilage of wine.
It is here where Pasteur discovered that bacteria can operate in an environment without oxygen, leading him to coin the term ‘anaerobic’ bacteria.
To address the problem with the spoiling (e.g. souring) of liquor, Pasteur discovered that the wine can be heated to around 60-80 degrees celsius to kill the microbes for 1-2 hours followed by immediate sealing of the liquor was suffice to slow down the spoilage of wine by a considerable degree. This process was later named Pasteurisation.
Therefore, wine can be preserved for long periods of time. If any higher temperature was used, it would destroy the wine/beer which is undesirable.
This is because by heating the wine, some of the non-pathogenic (non-infectious) micro-organisms are also eliminated from the wine. This effectively extends the shelf life of the wine and beer.
The same technique was applied to the beer and milk industry to prevent the spoilage of beer and souring of milk.
After his works on Pasteurisation, he was called to rescue the silk industry where silkworm were dying.
He worked on this day and night whilst tormented by the tragic death of his father and daughters that also occurred during this time. In short, he eventually examined the moths that were responsible for producing worms and found that small spores under the skin of silkworms was a prominent symptom for the disease.
At this moment, Pasteur hypothesised that the disease causing the premature death of silkworm’s egg (pebrine) is hereditary.
He produced two different groups of silkworms using the eggs of healthy moths and the eggs of diseased (with spores under their skin) moths
In the next spring, the eggs from healthy moths produced healthy silkworms whereas the eggs from diseased moths produced diseases silkworms.
At this point, Pasteur confirmed his hypothesis that the pebrine disease is hereditary.
Pasteur assisted with the cultivation of non-diseased moths and distribute the healthy eggs to produce healthy silkworms to farmers.
From here, Pasteur moved into anthrax disease that was devastating the wool industry in Europe. Pasteur investigated with injecting a weakened strain of bacteria responsible for causing anthrax into 14 sheeps in a laboratory. The results was that the vaccine (weakened or dead strain of pathogen) successfully provided the test sheep with resistance from being infected with anthrax.
This was put on a public trial when a famous veterinarian disagree with Pasteur about his results, mentioning that he yielded different set of results to Pasteur.
A test was performed in public where a lethal volume of anthrax was inserted into 25 of vaccinated sheep as well as another group of 25 sheep that were not vaccinated (acting as the control group). A few days later, all of the unvaccinated sheeps were killed while the vaccinated sheeps survived. This proved the succeed to vaccines in providing resistance to pathogens.
From his experiments with vaccines, Pasteur established the Principle of Immunity of using vaccines to provide immunity against diseases as well as the Germ Theory of Disease where germs (which we call pathogens today) are responsible for causing disease.
He later worked in creating vaccines for cholera in chickens, swine fever, rabies many more.
Learning Objective #3 - Assess the causes and effects of diseases on agricultural production, including but not limited to:
- Plant diseases
- Animal diseases
Plant diseases
A plant disease can be broadly defined as an abnormal condition that harms a plant thus lowering its productivity or usefulness.
There are two classes of plant disease – infectious and non-infectious.
In general, in order for a plant disease to occur, there must be:
1. A pathogen.
2. A susceptible host.
3. A favourable environment for pathogen to reproduce or replicate.
In order to transmit the disease from one affected organism to another, a mode of transmission of the pathogen is required. Sometimes, an organism acting as vector must be present to carry the pathogen (e.g. virus) from an affected host to an unaffected host. Therefore, in such scenario, the vector will be acting as the mode of transmission of pathogen.
Infectious Plant Disease caused by Fungi
The most common form of infectious plant disease is caused by the fungi pathogen.
We have already talked about how a fungus is able to produce spores in Module 5, so we will skip that process. Fast to when a fungus spore makes contact with a plant’s surface, it is able to germinate provided that the ambient environmental conditions are favourable for germination (e.g. sufficient moisture and nutrition).
Upon germination, the hyphae is able to emerge from the spore and enter the plant via their stomata on the underside of the leaves or penetrating through the epidermal cells on the leaves.
If the fungus successful invades the plant’s vascular system and cells, it is able to consume the plant’s nutrients. This thereby allows the fungus to undergo further reproduction, eventually spreading a lot pathogen (fungus) in the plant.
Also, the hyphae that are present outside the plant cell has contact with nutrients due to successful invasion and so it can produce spores (as we have explored in Module 5) which also helps the spreading of the pathogen to other plants.
The powdery mildew plant disease is caused by a fungus and can infect a plant (and cause plant disease) using the mechanism described above.
The result of the disease is defoliating and wilting the plants’ leaves. This reduces the potential for the plant to photosynthesis and produce peas.
Effect on agricultural industry: This has a serious implication on field peas grown in Victoria, resulting in the death of field pea plants. This can result the yield of peas up to 20%.
This reduces the yield of apples and pears for farmers.
Reduction in revenue for farmers.
Consumers will have experience an increase in fruit prices, lowering affordability.
Country may lose international trade opportunities as trading countries are charged a higher import price.
Infectious Plant Disease caused by Bacteria
In the case of fungi, the pathogen were able to breakthrough the epidermal cells of the plant directly.
The bacteria pathogen, however, is not able to do this.
Instead, bacteria is able to invade the host plant via the stomata or other openings such as wounds on the plant. To do this, water (must be present on the plant’s surface (e.g. from rain) so that the bacteria can move into the opening and enter the vascular systems.
It is inside the vascular system whereby the environment is favourable for the bacteria to reproduce via binary fission, creating bacterial colonies. These bacteria may produce toxins or proteins that are able to decompose plant tissue which the pathogen can use as nutrient for reproduction.
The bacteria responsible for causing plant disease can be transported by rain, wind or by pollinating insects.
A named example of a infectious plant disease that is caused by bacteria is Fire Blight.
This disease is commonly experienced by apples and pears.
The fire blight often starts with bacteria being sheltered in holes (known as cankers) in wood. When spring season (warm and wet) comes around, the bacteria can be transported from cankers to flower via water, wind or insects.
As a result of the flower carrying the infection across the branches and shoot, cankers are formed on the stem of the plant and the blights are formed on shoots due to death of cells and tissues. The dead leaves usually turn black, giving them a burnt appearance – hence the term ‘fire blight’.
This infection increases in scale, the cambium tissue consisting of the xylem and phloem will die which can result in the eventual death of the entire plant including fruits, if infection is not cured.
Sometimes you see bacteria flowing out of the fruit, in the form of a liquid/ooze, or flowing out of the cankers as the bacteria multiply during spring.
Effect on agricultural production:
As previous scenario involving Fungi.
Infectious Plant Disease caused by Virus
The Tomato Spotted Wilt is a plant disease that affects thousands of different plant species and not just tomatoes. It was named Tomato because it was the first recorded plant to be affected by such virus.
The virus pathogen is transported to the plant’s surface via thrips (a black-coloured insect). Therefore, the virus can make contact with the plant when the insect feeds on the tomato plant.
For virus to affect a plant, usually a vector (e.g. insects) is required rather than carried by wind and water.
Within a cell, the virus’s genetic material (RNA or DNA) is replicated. After some time, replicated virus can breakthrough cell membrane and spread to other cells in the plant or exit the plant an infect other plants.
This process degrades the fruit or crop’s quality and should not be consume due to potential of viral infection.
The symptoms experienced by the plant that is affected by the tomato spotted wilt virus include:
Wilting of leaves
Ringspots on leaves and fruit
Effect on Agricultural Production: Same as the case involving Fungi.
Animal diseases
Club Lamb Fungus Disease (Lumpy Wool Disease)
Cause of the Highly Contagious Disease
The Club Lamb Fungus is responsible for the case of this disease.
The fungus’ hypha is able to penetrate skin pores or hair follicles in sheeps. If the sheep is cut during wool shaving, it serves as another natural opening for the fungi to invade the sheep (where the sheep then becomes the host organism).
This fungus requires will take organic molecules from the sheep as their nutrient source (energy) for survival.
In other cases, the frequency of washing the sheep would also increase the susceptibility of the animal to Club Lamb Fungus . This is because water strips away the surface protective oil present on the sheep’s skin (e.g. lanolin).
As the fungus invasion takes a circular path, ring-shaped sores appear on the sheep’s skin.
Transmission of Disease
Affected sheeps will rub themselves on barn gates and walls.
Furthermore, sheeps that chew the wood in the barn will provide a moist environment for fungi spores to germinate and include hypha which can produce more spores.
Therefore, sheeps at exhibitions or sale market are susceptible to contracting the disease. This is because the fungi spore that may be present in wooden barn walls, soil and grooming tools can survive for long period of time (years) and germinate upon contact with a sheep.
Direct contact between affected and unaffected sheeps can also result in the transfer of spores.
Symptoms
Red, circular Lesions appear on the surface of the skin resulting hair loss in the centre of lesion.
These lesions will grow in size and eventually become scaly.
Loss of wool.
Clumping of wool.
Effect on Agricultural Production:
Reduce the yield of chicken due to death.
Consumers experience an increase in price, lowering affordability.
Decrease in revenue for farmers.
Reduce international trading opportunities due to high import prices experienced by countries.
Marek's Disease
Cause of Highly Contagious Disease
The Marek’s disease is caused by the Alphaherpesvirinae Virus which affect many birds such as chickens and turkeys. The bird can become affected by inhaling the virus.
Transmission
Affected chicken shred their dander (dead cells on the underside of feathers) containing the virus around 2 weeks after infection. When these infectious dead cells are inhaled by other chickens, they can be contracted with Marek’s disease.
The danders can spread via wind (i.e. air) too.
Once the chicken or bird has been affected with the disease, it will have it for the rest of its life and there is no existing treatment for such disease.
It is possible for the disease to transferred to turkeys.
Symptoms
Paralysis of chicken legs.
Tumours forming in feather follicles and organs.
Sometimes no observable symptoms are shown prior to the death of chicken.
Effect on Agricultural Production
Same as Club Lamb Fungus Disease.
Can effect other bird species which can lower their yields too.
Learning Objective #4 - Compare the adaptations of different pathogens to facilitate their entry into and transmission between hosts
Pathogen Adaptation for Entrance into Host
Prions
The normal prion protein (PrPC) is able to bind to the surface of a neuron to form a synapse with another neuron.
NOTE: Each neuron in the brain is capable of forming thousands of synpases to connect with thousands of other neurons.
However, the misfolded prion protein (PrPSC) is also able to bind to the surface of a neuron, resulting in neuron synapse degradation and eventually cell death.
Abnormal prion proteins are also able to activate enzymes that converts normal prion proteins into misfolded, dangerous prion proteins (PrPSC). This therefore results further neuron synapse degradation.
Therefore, misfolded or abnormal prions are infectious.
As misfolded prions are resistant to being denatured by high temperature, high pressure, UV radiation, digestion by lysosomes and toxic chemicals, they are not easily denatured in the body.
B cells or B lymphocytes can secrete protein that allows prions to enter and accumulate in follicular dendritic cells through which prions can invade the brain via peripheral nerves.
NOTE: The exact mechanism in which prion enters the blood-brain barrier is currently uncertain.
Misfolded prions present in meat can also bind with ferritin present in the meat so that the pathogen to move through intestines of the individual who consumed the meat.
As we have mentioned in Learning Objective #1, there are currently three known ways in an organism can be affected by a prion-caused disease. These are:
Inheriting a mutated Prnp gene from parent
Being exposed & acquiring the prion protein directly from the surrounding environment (e.g. oral ingestion, blood transfusion, contaminated surgical instruments, etc)
Developing the prion protein spontaneously (e.g. spontaneous DNA mutation or random misfolding of protein by chance resulting in a prion protein).
Viruses
Recall from Learning Objective #1, we mentioned that depending on the virus, it can either contain viral DNA or RNA as their genetic information.
For the virus that contains DNA information, they need to travel and penetrate the cell nucleus in order for replication to occur successfully. Comparatively, the virus that contains RNA as genetic information can replicate if they reach the cytoplasm or cytosol.
In either cases, the virus or the virus’ genetic information must pass through the cell membrane.
Let’s see how this can be done.
Generally, a virus can enter or invade a host cell in three steps:
First, the virus will be required to make contact via electrostatics to the host cell’s surface.
In the second stage, the virus’ own proteins (from its protein coat) will bind to one or more specific surface receptor belonging to either proteins, lipids or carbohydrates on the host cells’ surface or membrane.
NOTE: It is possible for different types of virus to bind to the same surface protein receptor as long as they’re matching with each other.
NOTE: In animals, the surface receptor must be specific to the virus and vice versa in order for successfully binding to occur. In plants, it is possible for virus to invade cell surface directly without the need of surface receptors.
Upon successful binding, the virus is able to transported through the membrane via the receptor mediated endocytosis or via a non-endocytotic pathway.
In receptor-mediated endocytosis, the virus bonded to the host cell’s receptor is enclosed by the cell as an endosome forms around the virus. The virus can then travel to the cytoplasm inside the endosome. At the cytoplasm, the virus can unwrap its protein coat and releases its genetic information.
In non-endocytotic pathway, after binding, the virus fuses with the cell membrane and only the genetic information of the virus is passed through to the cell membrane and into the cytoplasm.
If the genetic information is RNA, in the cytoplasm, protein synthesis occurs to produce protein coats to envelope around replicating RNA molecules.
We will not cover viral RNA replication as it is ourself the scope of HSC Biology.
An alternative pathway is that the virus can inject its genetic information (e.g. viral DNA) into the cell after successful binding. The viral DNA is subsequently able to direct the host cell to replicate the viral DNA and protein coat to contain these new viral DNA molecules. When the quantities of viruses becomes great enough, they will rupture the host cell and infect other cells in the host organism.
Interesting Note: HIV Viruses are retroviruses which mean they don’t have DNA, but RNA instead. So, they use an enzyme called reverse transcriptase to produce DNA from RNA. The role of this viral DNA is similar to what is discussed above for other viruses – i.e. the viral DNA gets replicated and eventually spread to other cells.
Bacteria
Unlike virus, bacteria cannot enter via receptor-meditate endocytosis due to their significantly larger size. For such reasons, the pathogen must cross the cell membrane and into the host’s cell via another pathway.
One of this pathway would be phagocytosis.
NOTE: As phagocytosis is mechanism responsible in our body’s 2nd line of defence, we will explore it in more detail when we look into the immune response system in the upcoming weeks.
Phagocytosis is the process whereby macrophages engulfs the pathogen (in this case the bacteria). Bacteria basically entices the cell to engulf them which allows the bacteria to bypass the cell membrane. In some bacteria, they have acquired adaptation where its outer capsule layer is able to survive and replicate within macrophages after phagocytosis.
An example of this occurs in the bacteria called Mycobacterium tuberculosis which responsible for Tuberculosis.
A secondary method for a bacteria to invade the cell membrane involves extensions on the bacteria known as Pili or Fimbria binding with the host cells’ surface receptor proteins that are matching (similar to the case of virus).
Once attached, the bacteria can secrete toxins that can break down connective tissue between cells on cell membrane allowing bacteria to pass through the cell membrane.
For instance, the Staphylococcus aureus bacteria is able to secrete chemicals (Hyaluronidase) to break down connective tissues and its responsible for skin infections.
Another pathway in which the bacteria can invade a host is by the presence of adhesion proteins on the bacteria surface. These adhesion protein can result in the adhesion receptors on the cell membrane to enclose part of the bacteria cell.
Protozoans
On the surface of the protozoan’s apex, there are receptors that can bind with host cell’s surface or cell membrane. These surface proteins present on protozoan are called antigens that is able to bind with sulphated glycosaminoglycan on the host cell’s surface.
After successfully binding, to invade the cell membrane, the protozoan has micronemes (organelle) that secretes adhesive proteins to strengthen the attachment to host cell for helical gliding (next step).
Next, a process known as helical gliding is performed by the protozoan to corkscrew itself through the cell membrane.
The mechanism through which helical gliding works facilitated by the: Actin–myosin motor complex
Subsequently, granule proteins are released to form a vacuole that envelopes and protect the protozoan from lysosome digestion.
Fungi
When a fungi spore germinates upon contact with surface that has moisture (and preferably cool temperature), hyphae can be released from the spore. The hyphae is able to penetrate the host cell’s membrane. They can do this because they have evolved to inherit structural adaptation called appressoria grown from the spore which are specialised organs that are capable of growing narrow infectious ‘pegs’ that applies great pressure at a small surface area, penetrating the cell membrane. In plants’ case, the pegs can penetrate the cuticle and epidermis cells.
NOTE: These pegs can then grow or produce haustoria, which are narrow projections that is capable of the host’s tissues in different directions, and obtain nutrients for the fungi’s survival.
Fungi’s hyphae can also adapted to have to the ability to secrete necrotic factors which are enzymes that can break down a portion of the cell membrane. This effectively allows the hypha to enter the host cell’s cytoplasm.
In plants’ cases, cuticle and cell wall layers are broken down by the release of enzymes in a sequential order. For instance, cutinase is secreted first to break down cuticle followed by cellulase to break down other layers such as epidermis cells.
Fungi have heat shock proteins that allows them to tolerate body temperatures of 37 degrees celsius.
Fungi have acquired adaptation in developing cell wall and capsule that allow some of them to survive and continue to produce spores when engulfed by macrophages.
Fungi’s hypha can also also enter via stomata on the underside of plant leaves. Other natural openings include hydathodes (pores on leaves), Lenticels (pores on plant barks that help gas exchange) and any plant wounds that came from insect bites, high temperatures, hail, wind, frost or even human.
Macro-Parasites
The Australian paralysis tick is an example of a macroparasite.
They can inject their mouth through the cell membrane and secrete saliva and neurotoxins into the cytoplasm. The salvia contain chemicals that stop mechanisms used to initiate inflammation response by the host.
The neurotoxins can cause temporary paralysis. In severe cases, the toxin can result in different forms of heart problems or failure.
Hookworms larvae are able to penetrate the skin such as between toes via hair follicles. Upon successful entry, they will be carried to the heart and lungs via blood. Upon coughing and swallowing, they will enter the small intestines where they mature and develop eggs. It is through the individual’s faeces (poop) where the eggs or larvae of the hookworms are be secreted.
During the time hookworm remains in the body and intestines, it can cause many disease such as by penetrating intestinal walls.
Hookworms are able to produce immunomodulatory proteins that hinders the B and T lymphocytes from attacking the pathogen.
NOTE: As we have mentioned in Learning Objective #1, Macro-Parasites can act as a vectors for pathogens like virus and bacteria.
Different transmission pathway for pathogens due to Adaptation
Adaptations for Water Transmission:
Some pathogens that are transmitted via water are chlorine resistant meaning that chlorination by water treatment plants to produce potable (drinkable) water to households will not kill these chlorine resistant bacteria. Elaborate filtration will need to be used if these bacteria are causing dangerous diseases.
EXAMPLE: Staphylococcus aureus (Bacteria) and Aeromonas hydrophilia (Bacteria)
Ability to not be dissolved in water (i.e. survive) and reproduce in water.
Ability to move through water such as using structures like Pili (Fimbria) and flagellum in the case of protozoans and bacteria.
Adaptations for Air Transmission via water droplets:
There are pathogens that can survive the acidic environment of stomach by secreting enzymes that enable it to convert urea in the blood into ammonia. This allows them to survive, cause diseases such as peptic ulcers and also be able to exit the affected host and affect a new host via water droplets (e.g. sneezing).
Example: Heliobacter Pylori (Bacteria)
NOTE: This means that they can alter the affected organism’s behaviour by causing sneezing to facilitate their transmission.
These pathogens are capable of floating in air due to light weight.
They should be able to survive in water droplets as it is a pathway in which they can infect a new host.
These pathogens does not dry out due to wind.
Adaptations for Faeces – Oral transmission:
Endoparasites are pathogens that are able to tolerate and survive in environments in the body (i.e. alkaline pH and low oxygen of animal intestines)
Ability to cause diarrhoea in animals to cause the secretion of pathogen larvae (eggs) to transmit disease to new host.
NOTE: This means that they can alter the affected organism’s behaviour by causing sneezing to facilitate their transmission.
Some of these pathogens have genes that produces proteins that allows it to be resistant to chemicals ingested by the host designed to kill the pathogen.
Adaptations for Vector-assisted transmission:
Pathogen’s structural integrity and capacity to act as an infectious organism or agent are not affected when absorbed by or bound to vector. Therefore, they have adapted to survive inside vector’s body.
Example: Plasmodium (a protozoan) has adapted living in the Anopheles mosquito species.
Some pathogens have surface receptor proteins that can attach to vector. Also, these Pili and adhesion proteins can attach to host cells as we have explored in the previous section. This allows them to not be washed away as it moves through the intestines and released with organism’s urine.
Example: Pili and adhesion proteins on Bacteria
The maturation of eggs to become infectious agents of some pathogens are similar to vector’s feeding times.
Adaptations for Sexual transmission:
Ability to enter the uterus.
Able to survive in placenta and transmit transmit disease when organism consume placenta.
Example: HIV Virus