Download to view a sample chapter of SACE1 Biology

FIRST EDITION
Australian Curriculum
Alan Crierie, David Greig, Simon Ruthven
T
SACE 1
AF
Biology
D
R
WORKBOOK A
Topics 1 & 2
STAGE 1 BIOLOGY WORKBOOK A
TABLE OF CONTENTS
Table of Contents
Frontmatter
Topic 1 Cells and microorganisms
Chapter 1.1 Living things consist of cells
Chapter 1.2 Two major types of cells
T
Chapter 1.3 Cell division
Chapter 1.4 Cell requirements
Chapter 1.5 The cell membrane
Chapter 1.6 The importance of microorganisms
AF
Chapter 1.7 Microorganisms and food
Chapter Appendices (Answers and Laboratory Notes)
Topic 2
Infectious Disease
Chapter 2.1 Infectious Disease differs from other diseases
Chapter 2.2 Disease transmission
Chapter 2.3 Epidemics and other health issues
R
Chapter 2.4 Disease Control
Chapter 2.5 Adaptations of pathogens
Chapter 2.6 Physical barriers to disease
Chapter 2.7 The innate immune system
D
Chapter 2.8 The adaptive immune system
Chapter Appendices (Answers and Laboratory Notes)
General Appendix (Student and Teacher resource materials)
Glossary of Key Terms
TOPIC 2
INFECTIOUS DSEASE
Chapter 2.5 Adaptations of pathogens
Understanding
Pathogens have adaptations that facilitate their entry into the cells and tissues of hosts.
•
Describe how pathogens and host cells recognise each other.
•
Explain that some pathogens enter cells to survive and reproduce.
•
Describe the basic concept of molecular recognition, e.g. pathogens binding to cellular receptors.
•
Explain that some pathogens must enter cells to ensure their survival replication, and to evade the immune
system.
© SACE 2016
T
In Chapters 2.1 and 2.2, pathogens that give rise to infectious disease were examined in some detail. To
cause disease all pathogens must colonise their specific host, avoid immune systems, multiply and then be
able to spread themselves to other hosts.
Many pathogens are termed intracellular as they enter cells and it is here that they survive and multiply. The
ability to cause disease in a host is called pathogenicity and virulence is the degree to which the pathogen
causes disease. A pathogen with high virulence has properties that enable it to bring about a high level of
disease in a host.
•
•
•
•
AF
Humans are vulnerable to penetration by pathogens in four main ways:
respiratory surfaces
wounds
digestive system
reproductive organs
Refer to Figure 251 which illustrates how humans can be vulnerable to pathogen entry.
Entry points for pathogens
R
Respiratory surfaces
air borne pathogens may
enter the mouth and
nose and be absorbed
across mucous membranes
of the respiratory surfaces
D
Wounds
the skin generally provides
a good proctive barrier to
microbes but if skin is
broken, as in a cut, then
pathogens can enter
Digestive system
if food is contaminated
then pathogens can enter
via the mouth and enter the
digestive system
Reproductive organs
urethra in males and females
and vagina in females
Sexually transmitted pathogens
can enter across mucous
membranes.
Figure 251 How microorganisms can enter the body
106
© Essentials Education 2016.
ADAPTATIONS OF PATHOGENS
CHAPTER 2.5
Adaptations
There are many adaptations processed by pathogens to facilitate their entry, survival and reproduction in
hosts.
Using a vector
Some pathogens manage to enter the bloodstream by using a vector to assist them. A rather large group of
microbes, including examples from bacteria, viruses and protists, have adapted to survive in certain insects
so they can be transferred to their hosts. The disease of malaria is spread in this way with the Plasmodium
organism being well adapted to living in certain species of mosquito.
Figure 252 shows a mosquito biting a human.
Attachment to host tissue
T
Many pathogens are well adapted, once inside the host, to attach to host cells so that food moving through
the intestines or the washing action of urine flow does not expel them from the body. They produce specific
proteins called adhesions that can recognise and bind in a complementary manner to molecules on host cells.
An assignment is provided at the end of this Chapter to help you understand this.
AF
Figure 253 shows surface projections (pili) that have proteins at the tip that can bind to cell receptors.
Figure 252 A mosquito biting a human
Figure 253 E. coli bacterium showing pili
R
Ability to withstand harsh environments
The human stomach provides a particularly harsh environment for pathogens; it contains acid with pH 2,
thick mucous layers and continual churning action. Nonetheless, a bacteria, Heliobacter pylori, which can
cause stomach ulcers can survive and reproduce. One of its adaptations is its ability to secrete an enzyme
which converts urea to ammonia which helps to combat the acidic environment.
Biofilms
D
More than 99% of bacteria exist in colonies known as
biofilms, adopting a range of unique properties such as
existing in a dormant state with reduced metabolism,
becoming resistant by transferring genetic information
within the colony and preventing antibiotic penetration by
surrounding themselves in a slime-like matrix. All of these
factors result in biofilm bacteria being difficult to identify
using standard culture-based methods and resistant to
traditional antibiotic therapy.
One particular bacterium, Staph. aureus is known to
cause many sinus infections and is very difficult to treat
with antibiotics. See Figure 254.
Figure 254 Staph areus and a biofilm
© Essentials Education 2016
107
TOPIC 2
INFECTIOUS DSEASE
Producing toxins
It is often noticed that microbes may employ more than one specific adaptation to assist in their survival. In
the above example of the bacteria H. pylori, they secrete adhesion molecules and also produce toxins that
destroy the cells lining the stomach, thereby causing an ulcer.
Another bacterium, Bordetella pertussis, which causes whooping cough also produces toxins which destroy
cells lining the respiratory tract which reduces the infected person’s chance of clearing the infection.
Binding to molecules on the surface of host cells
Nearly all intracellular pathogens need to bind to receptor molecules on the surface of the host cells. This
concept has already been described with the production of adhesion molecules produced by bacteria.
T
Virus particles possess surface molecules that can bind in a complementary manner with surface receptor
molecules and this enables them, in many instances to be taken into the cell. Viral infection, including uptake
and replication is examined later in this Chapter. Refer to Figure 255.
protein
AF
RNA
lipid bilayer
cell receptor
Figure 255 A virus binding to cell receptors
Figure 256 An example of phagocytosis
Ability to survive inside white blood cells
R
Tuberculosis is caused by the bacterium Mycobacterium tuberculosis. It is taken into the lungs and from
here white blood cells engulf the bacteria. The body’s immune system contains the infection within a lesion
(tubercule) and it is known that the pathogen can survive inside the white cells inside the lesion for decades.
The bacteria that causes Legionnaires disease has a similar adaptation. Figure 256 shows a white blood cell
engulfing a bacterium by phagocytosis.
Altering the behaviour of the host organism
Pathogens may alter the behaviour of their host which may assist in the spread of the microbe to other hosts.
Two examples of this type of action are:
Inducing diarrhoea; whilst this may flush some bacteria from the gut assisting the host, it also enables
infections to spread via contaminated water. (e.g. cholera)
• Coughing and sneezing with colds or influenza will expel virus particles in tiny droplets which may then
be inhaled by others to cause the spread of the disease.
It has been estimated that in one sneeze there may be up to 20,000 droplets and if the person is infected
D
•
with rhinovirus this may be thousands of viral particles.
Changing antigens on the surface of the microbe
Antigens on the surface of pathogens are the molecules that are recognised by the host organism and
represent a critical phase in the recognition and destruction of the invading organism. One powerful
adaptation of many bacteria and viruses is their ability to change their outer antigen configuration to help
evade the human’s immune system. This concept will be discussed further in coming chapters.
108
© Essentials Education 2016.
CHAPTER 2.5
ADAPTATIONS OF PATHOGENS
Drug resistance
Chapter 2.3 examined the ability of bacteria to develop resistance to antibiotics, with this looming as one of
the most significant threats to human health in the coming decades. Superbugs is a term coined to describe
the new strains of bacteria that are resistant to all known antibiotics.
Avoiding white blood cells (phagocytes)
Figure 256 illustrated a white blood cell, called a phagocyte, engulfing a bacterium with the aim of destroying
it. Most bacteria that are successful as pathogens have evolved ways to avoid being engulfed by these white
blood cells.
Viral replication
T
Virus particles are not cellular, they do not display many properties of other microbes but they can enter a
host cell and use the host’s DNA and ribosomes to make new viral particles that can leave the cell and
infect other cells in either the same or other hosts. As such, viruses lack the necessary organelles such
as ribosomes to make protein molecules. Viruses are specific in the cells they infect, this is determined by
the complementary binding between their surface antigens and host receptor molecules. Refer again to
figure 255.
AF
Refer to Figure 257 which illustrates the five general steps of the viral reproductive cycle. In the process of
transcription, DNA is used to make a molecule of mRNA (messenger RNA). mRNA can be used to make
viral protein molecules on organelles called ribosomes, this is called translation. Copies of viral DNA can be
replicated to make more copies, using host cell chemicals and energy.
Attachment of the virus 1
to complementary surface
receptor molecules
on the cells surface
Virion
2
Virus moves
into the cell
by endocytosis
Transcription
R
Cytoplasm
Replication of 3
viral DNA using
host DNA
5
Package and assembling of
new virus particles
Translation
D
Synthesis of new viral
components using
host cell ribosomes
4
Figure 257 The five general steps of the viral reproductive cycle
Helpful Online RESOURCES about viral replication
Use this QR code to jump to our website which will provide an EVA about viral reproduction:
<http://essentialseducation.com.au/resources/sace-1/biology/viral-replication/>
© Essentials Education 2016
109
TOPIC 2
INFECTIOUS DSEASE
Human Endeavour EXERCISE 2.5 - The HIV/AIDS drug AZT
The drug AZT has been used since about 1987 in the treatment of HIV infection.
Do some research and write concise answers to the following questions.
1.
Explain how the drug works to reduce the symptoms of the disease.
2.
State reasons why the drug is not 100% successful in eliminating the virus.
3.
Describe and state reasons for a complication or side effect of using the drug.
4.
Explain one way in which HIV can change to develop resistance to the drug
Use your own paper or a screen as directed by your teacher.
Helpful Online RESOURCES about AZT
<http://www.britannica.com/science/AZT>
Plant pathogens
T
Use this QR code to jump to the website below which will provide a valuable start in your
research for this Assignment:
Fungi
AF
Organisms that can bring about plant disease are again many and varied and include pathogens such as
fungi, bacteria, viruses and viroids and nematodes.
Fungal pathogens can infect plant tissue and obtain nutrients from the plants cells. Figure 258 (a) shows
‘Tomato Blight’ a fungal infection of tomato leaves.
Phytophthora root rot is caused by the soil fungus Phytophthora cinnamomi. This disease can affect native
plants and is a major threat to some rare and endangered species. The fungus often grows through the root
system and in the process destroys the plant’s ability to absorb water and nutrients. The fungus produces
spores which can survive for long periods of time in the soil.
The disease has spread over most of Australia and has been very difficult to diagnose and treat.
Methods of reducing the impact of Phytophthora include:
D
R
• quarantine-fencing off infected populations and reducing public access
• hygiene practices-e.g. sanitising tools and boots (see Figure 259 overpage)
• spraying infected plants
Figure 258 (b) illustrates dieback caused by Phytophthora.
Figure 258 (a) Tomato blight
110
Figure 258 (b) Phytophthera dieback
© Essentials Education 2016.
CHAPTER 2.5
ADAPTATIONS OF PATHOGENS
Figure 2510
Bacterial infection
Figure 2511
A nematode
T
Figure 259 (a) and (b) A boot cleaning station in a
National Park in Queensland
Bacteria
There are about 100 known species of disease-causing bacteria in plants. They bring about their pathogenicity
by producing toxins or other proteins that cause disease.
AF
Pseudomonas syringae causes tomato plants to yield less crop and has several adaptations to facilitate its
spread including the production of chemicals that help evade the tomato plants immune system. Figure 2510
shows an example of this bacterial infection.
Viruses and viroids
Viroids are smaller than virus particles and contain RNA. An example of one of the first of these to be
discovered was the potato spindle tuba viroids. Often plant viruses and viroids can be transmitted by a
vector.
Nematodes
Nematodes are small, wormlike creatures that have the capacity to cause significant damage to root cells
in plants. There are a number which infect food crops e.g. potatoes, cucumbers and strawberries. Figure
2511 illustrates a soil nematode.
R
Key Concepts
For pathogens to cause disease they need to:
•
•
•
•
2.
colonise the host
avoid the immune system
reproduce
spread to other hosts
Different pathogens or members of related species have different levels of virulence.
3.
Entry into human hosts is usually through:
•
•
•
•
4.
wounds
respiratory surfaces
reproductive organs
digestive system
Pathogens have evolved a vast range of adaptations that enable them to survive and spread
including hiding inside cells.
5.
Viruses use the host cells enzymes, nucleic acids and organelles to produce new viral particles.
6.
Plants are also highly susceptible to pathogens which cause major problems to the agricultural
industry.
D
1.
© Essentials Education 2016
111
TOPIC 2
INFECTIOUS DSEASE
What have you learned?
Key terms
immune system
adaptations
complementary binding
receptor molecules
pili
toxin
intracellular
transcription
T
translation
phagocyte
rhinovirus
ribosomes
AF
antigen
pathogenicity
virulence
viroids
nematodes
Knowledge and Understanding
Name three ways that pathogens enter the human body and give an example of a pathogen for each.
R
1.
State the difference between pathogenicity and virulence.
D
2.
112
© Essentials Education 2016.
ADAPTATIONS OF PATHOGENS
3.
CHAPTER 2.5
Pathogens have a range of adaptations to assist them in entering, reproducing and exiting hosts.
Complete the following table regarding the type of adaptation, how it provides an advantage and an
example of a pathogen that possesses such an adaptation.
Adaptation
Description of how the
adaptation works
Example
Using a vector
Attachment to host cells to avoid
being flushed out of host
Helicobacter pylori
Production of toxins
Describe how fungal spores provide a reproductive and/or survival advantage to those species that
produce them.
AF
4.
T
Hiding inside host cells
Application, Analysis and Evaluation
Compare two pathogens; one with high virulence and one with low virulence. Explain the features that
contribute to the virulence.
6.
High virulence can be seen as a disadvantage to the pathogen. Explain the reasons for this.
R
5.
Compare and contrast two methods for controlling the spread of the plant fungus Phytophthera.
8.
Causing diarrhoea can be seen as an advantage for both the host and pathogen. Argue how this is
possible.
9.
Show how a pathogen gains an advantage by hiding inside a host cell.
D
7.
© Essentials Education 2016
113
TOPIC 2
INFECTIOUS DSEASE
Extension
10. Select a pathogen which infects a plant of direct commercial value such as a plant that is used for food
or fibre. Do some research on this topic to answer the following questions.
a)
How is this pathogen transmitted to the plant?
b)
What are the symptoms displayed by the plant when infected?
c)
What is the commercial impact of this disease on the crop that is produced?
d)
What treatment and/or management plan is used in order to try to minimise the effect of this
disease?
Present your report according to the guidelines given by your teacher.
T
Helpful Online RESOURCES for plant diseases
Use this QR code to jump to the website below which will provide a valuable start in your
research about plant diseases:
<https://en.wikipedia.org/wiki/Category:Plant_pathogens_and_disease>
AF
Human Endeavour ASSIGNMENT 2.5 The profile of a ‘real ‘scientist
Carefully read the profile of Dr. Donald Gardiner, a plant pathology scientist, who grew up and went
to school in Adelaide and now works with the CSIRO in Brisbane. See next page. Discuss how his
work (and his colleagues in other laboratories) exemplifies the following aspects of ‘Science as a
Human Endeavour’. You may wish to consult the SACE syllabus statement for more detail about
each of the headings below. You may need to do some research into CSIRO and other large research
organisations.
Your teacher will provide more information about the details of your report .
1.
Communication and collaboration
a)
b)
2.
Science is a global enterprise
International collaboration
Development
Development of complex scientific models and/or theories
R
a)
b)
3.
Influence
a)
Advances in one field can influence other areas of science
b)
The use of scientific knowledge can be influenced by other considerations
Application and limitation
D
4.
New technologies
a)
Scientific knowledge can be very widely used
b)
The use of scientific knowledge may have beneficial or unexpected consequences
c)
Science informs public debate and is in turn influenced by public debate
Helpful Online RESOURCES for CSIRO
Use this QR code to jump to the website below which will take you to CSIRO and provide
a valuable start in your research for this Human Endeavour Assignment:
<http://www.csiro.au/en/Research/AF>
114
© Essentials Education 2016.
ADAPTATIONS OF PATHOGENS
CHAPTER 2.5
PROFILE for Human Endeavour ASSIGNMENT 2.5
Dr. Donald Gardiner
My work aims to understand how a group of the most devastating
fungal pathogens of wheat invades their host plant. The pathogens
are called Fusarium graminearum and its close relative, Fusarium
pseudograminearum. During infection they produce a toxin, called
deoxynivalenol, which both assists with invasion of the plant and also
contaminates any grain that is harvested from the crop. This toxin is highly
harmful to humans and animals that may eat the grain. By understanding
the mechanisms a pathogen uses to cause disease, we hope to be able
to implement better control strategies that will assist the farmer to protect
their crops and deliver safer food to consumers.
T
In modern molecular biology, having a genome sequence for your organism
of interest is highly advantageous. With new DNA sequencing technology,
obtaining genomes for fungi is relatively straight forward. However, the way the genome sequence is
obtained means it remains in literally millions of pieces that need to be put back together and this can
be a challenging task. With advanced software and high performance computing, we can now put
most of these pieces back together. For our Fusarium species ,when this is done we typically end up
with genomes in about 500 pieces.
AF
Each of these pieces will contain hundreds of different genes. By predicting the genes that are encoded
by the genomes we can begin to understand how the pathogen has evolved and the mechanisms
that it uses to invade its host. This is done by comparing all of the genes encoded by a pathogens
genome with those of both closely and distantly related organisms. The general term for approaches
like this is “comparative genomics”.
R
One of the most fundamental components of comparative genomics is the ability to compare the
sequence of the genes or proteins encoded by an organism’s genome. One tool that is extensively
used is BLAST; (basic local alignment search tool). I have previously used BLAST to compare the
entire gene set of many different genomes of fungi all at once. These comparisons can be used to
identify highly conserved genes, that might be important for basic cellular functions such as energy
generation or DNA replication, and genes that are less well conserved or only present in a few species.
It is this latter group that might contain genes involved in virulence on a particular plant host. Using
this approach we recently discovered genes in the genome of Fusarium pseudograminearum that
had been horizontally transferred between distantly related fungi that all shared a common plant
host (Gardiner, McDonald et al. 2012). In some example genes were also shown to be transferred
between bacteria and fungi.
To test the hypothesis that these genes (shared exclusively between pathogens with a common host)
are involved in virulence, mutant strains of the fungus are created and compared to the wild type
strain in plant infection assays. This is done by replacement of the gene with an antibiotic resistance
gene using homologous recombination. This creates a mutant organism that, apart from the deleted
gene and antibiotic resistance is identical to the original pathogen. These strains are then compared
for their ability to infect the host plant in a controlled environment room. Through this process we can
begin to understand how these fungi cause disease on wheat.
D
Education and career
I studied a Bachelor of Biotechnology (honours) at the Flinders University of South Australia and
completed a PhD in molecular plant pathology at Melbourne University where I researched the
interaction between canola and a fungal pathogen. After a brief post doctoral fellow at the University
of Queensland, undertaking research in mammalian genomics, I joined the Australian Commonwealth
Scientific and Industrial Research Organisation in 2005, where I have been researching Fusarium
incited diseases of a number of crop plants ever since.
Gardiner, D. M., M. C. McDonald, et al. (2012). “Comparative pathogenomics reveals horizontally
acquired novel virulence genes in fungi infecting cereal hosts.” PLoS Pathog 8(9): e1002952.
© Essentials Education 2016
115