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6/6/2016 Infectious Disease

Biological and drug defences

Nathan Hughes
97783
There are four organisms responsible for causing infectious diseases they are

Protozoans, Fungi, Bacteria, Viruses and Macroparasites.

A table to show the four organisms responsible for causing infectious


diseases in humans with a description and an example of the diseases they
can cause.

The 3 main types of protozoans (which means first animals) these are Amoeba,

Paramecium and Euglena, they are unicellular eukaryotic organisms. They need a

moist environment like water to survive. They reproduce asexually and sexually. They

feed heterotrophic. To provide movement Amoeba use a pseudopod (A false foot)

Paramecium are covered in cilia which wiggle to provide propulsion (similarly to how

a sting ray moves, just on a microscopic scale.) While Euglena have a flagellum which

wiggles to provide propulsion, they can detect light, and they are between 0.01 and

0.05 mm long, which is too small to be seen with the naked eye, therefore, simple

microscopes are needed to view them, however they can grow up to 3mm in length.

Protozoans can cause diseases such as Malaria and Toxoplasmosis to name but two.

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A diagram of an Amoeba protozoa and the Pseudopods

A diagram of a Paramecium protozoa and the Cillia

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A diagram of a Euglena protozoa and the Flagellum

Fungi are multicellular eukaryotic cells, they feed heterotrophic. Most are saprophytic.

They are Decomposers and recyclers. They are considered internal or external

parasites. They are non-motile and they lack true roots, stems and leaves. They need

warm, moist environments to survive. They reproduce asexually and sexually.

(Asexual reproduction is genetically identical.) they mainly use aerial dispersion to

spread spores. Tinea pedis is a fungal infection of the feet, it is due to a dermatophyte

fungus. Tinea pedis thrives in warm humid conditions and is most common in young

adult men. It is commonly treated with an antifungal medication such as miconazole.

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A picture to show the fungal infection Tinea pedis.

Bacteria are prokaryotic cells. Most prokaryotes are unicellular, although the cells of

some species remain attached to each other after cell division. Prokaryotic cells

typically have diameters of 0.55 m, much smaller than the 10100 m diameter of

many eukaryotic cells. (One notable exception, Thiomargarita namibiens is750 m in

diameter-bigger than the dot on this i.) Prokaryotic cells have a variety of shapes

although they are unicellular and small, prokaryotes are well organized, achieving all

of an organisms life functions within a single cell. A key feature of nearly all

prokaryotic cells is the cell wall, which maintains cell shape, protects the cell, and

prevents it from bursting in a hypotonic environment. In a hypertonic environment,

most prokaryotes lose water and shrink away from their wall (plasmolyze). Such water

losses can inhibit cell reproduction. Thus, salt can be used to preserve foods because

it causes food-spoiling prokaryotes to lose water, preventing them from rapidly

multiplying.

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A diagram of a bacterial prokaryote cell

Bacteria can cause humans many diseases such as Clostridium Botulinum, which is

the deadliest natural occurring substance known to mankind. Staphylococcus aureus,

which is a gram-positive coccal bacterium, that is frequently found in the nose,

respiratory tract, and on the surface of the skin. Although Staphylococcus aureus is

not always pathogenic, it is a common cause of skin infections such as abscesses,

respiratory infections such as sinusitis, and food poisoning and Salmonella which is a

genus of rod-shaped (bacillus) gram-negative bacteria. The Salmonella enterica

subspecies are found worldwide in all warm-blooded animals, and in the environment.

Strains of Salmonella cause illnesses such as typhoid fever, paratyphoid fever, and

food poisoning (salmonellosis).

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Viruses are the smallest of the microbes. Viruses are obligate parasites therefore they

must have a host in order to replicate. A typical virus particle has a single or double

strand of genetic material (nuclear acid - either DNA or RNA) surrounded by a shell

like coat of protein called a capsid and occasionally a protective outer envelope.

Viruses have three main shapes, spiral like a spring (Helical). Complex like a rocket

(bacteriophage) and Icosahedral which is 20 equal sided triangles that interconnect.

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A diagram to show the three main shapes of viruses.

Macroparasites are small organisms that can spread infectious diseases, some

examples are Head lice, Scabies, Ticks, Bedbugs and Tape worms. Many

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Macroparasites are considered vectors. Some examples of vector borne diseases

are, Malaria, Tick borne Typhus, Lyme Disease, Scabies & Rabies. With vector-borne

diseases the key feature is an animal or other medium to spread the disease from one

host to another.

An example of a Bedbug, a Head louse and a Deer tick all of which are

Macroparasites and vectors.

The diagram below shows the life cycle of a bed bug.

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The diagram below shows the life cycle of a head louse

In the case of Malaria, the vector is the female Anopheles mosquito, when they feed

on blood; the stylets on the end of the mosquitos proboscis pierce the skin and probe

for a blood vessel. While sucking the blood, the mosquito pumps saliva into the host,

this prevents the blood from clotting and acts as an anaesthetic to stop the host feeling

the mosquito. Male mosquitoes do not transmit the disease as they feed only on plant

juices.

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A picture of a mosquito with is a vector for parasite Plasmodium Vivax which
causes Malaria

The Plasmodium parasite has a complex life cycle characterized by alternating

extracellular and intracellular forms, involving sexual reproduction in the mosquito and

asexual reproduction in the liver cells and RBCs of humans.

The parasite enters the human host when an infected mosquito takes a blood meal.

Sporozoites from the mosquitos salivary glands are injected into the hosts

bloodstream. Within 30 minutes the sporozoites will have entered the hosts liver cells.

The sporozoites feed on the cells contents, grow and change to form schizonts. Over

the next 5-8 days they divide rapidly, forming thousands of merozoites. The liver cells

burst open, releasing merozoites into the bloodstream where they invade the RBCs.

(Red Blood Cells or erythrocytes). While the parasite is within the liver the person

does not feel sick and shows no signs or symptoms of the disease. Plasmodium vivax

can have a dormant stage in the liver called hypnozoites. These can remain in the liver

for several years, causing relapses in later life. While in the liver and the RBCs the

parasite is protected from the hosts antibodies.

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A diagram to show the Plasmodium life cycle.

Pathogens can enter the body via orifices (ears, mouth, reproductive system and eyes)

either by contact or indirect contact by vehicular transmission, or through the skin via

cuts and/or insect bites, or via the respiratory system from inhaling contaminated

waterborne droplets.

Three methods in which pathogens can be transmitted are direct contact between

people - touching, kissing, sexual intercourse. Vehicular transmission - where a

pathogen is carried on a non-living object, such as, food, water, airborne droplets from

a cough, sneeze or dirty nail. Vector transmission, where a pathogen is carried by an

insect such as malaria being carried by a mosquito.

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Humans have many barriers (first layer of defence against a pathogen) whether they

are physical, (such as the skin). Mechanical (the epithelial surfaces of the gut and

respiratory tract) or chemical (the tears in our eyes which have the enzyme lysozyme

in them. Our ear wax which has antimicrobial properties. The Stomach that contains

hydrochloric acid which has a high pH which pathogens cannot survive in. The large

intestine, urethra and vagina have resident harmless bacteria that use the nutrients

which harmful microbes would need to survive this causes the harmless bacteria out-

compete the harmful bacteria for space and nutrients. In addition, sweat covers areas

of the skin, it is an acidic liquid that contains enzymes which kills some bacteria.) which

a pathogen needs to bypass in order to gain access into our body. Once a barrier has

been bypassed phagocytosis, inflammation, interferons and fever take over (viral

infections only)

A diagram to show the multi layered approach of the immune system

Phagocytes are a type of white blood cell (lymphocyte) that engulfs pathogens in a

process known as phagocytosis. They are found in blood and tissues; They are the

first cells to respond to a pathogen inside the body. The Phagocytes recognises the

foreign antigens on a pathogen, the cytoplasm of the phagocyte moves round the

pathogen to engulf it, the pathogen is now contained in a phagocytic vacuole in the
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cytoplasm of the phagocyte. A Lysosome fuses with the phagocytic vacuole and

breaks down the pathogen by lysis. The phagocyte then presents the pathogens

antigens on its surface to activate T-cells. Lysozymes are enzymes that disrupt the

cell walls of gram positive bacteria by digesting the peptidoglycan. It is found in human

tears, saliva and lysosomes.

A diagram to show phagocytosis

Interferons are proteins produced by virus-infected body cells in response to the virus.

Interferons trigger the production of a second protein that inhibits viral replication, by

binding to mRNA coded by the virus.

The complement system is then activated. The complement system consists of a

group of approximately 30 serum proteins that activates inflammation, destroys cells

and participates in opsonisation. The complement system can be activated by a

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number of different foreign molecules. The complement proteins respond in a

sequential manner, producing a cascade of reactions.

The major components of the complement system are C1 through C9 named in the

order that they were discovered, not the order in which they function. The

complement-cascade can be activated by the Classical pathway, or by the Alternative

pathway.

In the Classical pathway C1 becomes activated when it binds to an antigen-antibody

complex, then the activated C1 cleaves C2 into C2a and C2b and C4 into C4a and

C4b. C2b and C4b combine to form a protease called C3 convertase, the C3

Convertase then cleaves C3 into C3a and C3b.

In the Alternative pathway, antigens such as endotoxin, polysaccharides or cell wall

components react with C3b. Small amounts of C3a and C3b are constantly being

formed from C3, but without activation, however, they are soon destroyed. C3b reacts

with the proteins Factor B, Factor D and Properdin to form a complex called C3

convertase, which cleaves C3 into C3a and C3b.

Both the Classical pathway and the Alternative pathway of complement system

activation follow the same sequence after cleavage of C3. It is the C3a that is involved

in stimulating inflammation.

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A diagram to show how the compliment system works.

A table to show the major components of the immune system to their role in
the specific immune response

These cells act as co-ordinators of the immune system. They


T-Helper Cell activate other cells of the immune system by releasing
interleukins.
These cells destroy infected cells or tumour cells by
Cytotoxic T-Cell
penetrating the cell membrane with a protein called perforin.
These cells differentiate into plasma cells, although some
B-Cell
eventually become memory cells.
These cells produce large numbers of antibodies which
Plasma Cell
neutralise pathogens and toxins.
These cells persist after an infection is gone. If stimulated by
Memory Cell a secondary exposure by the same organism, these divide
rapidly and produce a large secondary response.

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A diagram to show the main components of the immune system.

When a pathogen enters the host for the first time it activates the immune system, this

is the primary or humoral response. This response is slow because there arent many

B-Cells that can produce antibodies needed to bind to the pathogens antigens.

Eventually the host will produce enough antibodies to defeat the pathogen, the

infected host will show signs and symptoms of the disease during this phase. Both B

and T-Cells produce Memory Cells, these will remain in the host long after the

pathogen has been destroyed. Memory T-Cells remember the specific antigen

needed to recognise the pathogen on a second exposure. Memory B-Cells remember

the specific antibodies needed to bind to the antigen. The host now has the ability to

respond much more quickly to a second exposure.

If a secondary exposure by the same pathogen happens, the specific immune

response will produce a quicker, stronger response. Clonal selection happens faster.

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Memory B-Cells are activated and divide into Plasma Cells that produce the correct

antibody to the antigen. Memory T-Cells are activated and divide into the correct type

of T-Cells to kill the cell carrying antigen. The specific immune response often

destroys the pathogen before the host begins to show any symptoms (The host is

immune to that pathogen) this is known as acquired immunity.

The antigen receptors on B lymphocytes are identical to the binding sites of antibodies

that these lymphocytes manufacture once stimulated, except that the receptor

molecules have an extra tail that penetrates the cell membrane and anchors them to

the cell surface.

Antibodies (Ig) are proteins collectively known as immunoglobulins. They have the

same basic molecular structure, consisting of four polypeptide chains. Two of the

chains, which are identical, are heavy chains; the other two are identical light chains.

Each chain is encoded by different genes. The four chains are joined to form a flexible

Y shape, which is the simplest form an antibody can take.

At the tip of each arm there is an area called the antigen-binding, which is formed by

a portion of the heavy and light chains. Every immunoglobulin molecule has at least

two of these sites. The antigen-binding site is what allows the antibody to recognize a

specific part of the antigen. If the shape of the epitope corresponds to the shape of the

antigen-binding site, it can fit into the site. Chemical bonds called weak bonds then

form to hold the antigen within the binding site.

The heavy and light chains that make up each arm of the antibody are composed of

two regions, called constant and variable. These regions are distinguished on the

basis of amino acid, constant regions have essentially the same amino acid sequence

in all antibody molecules of the same class (There are five classes of

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immunoglobulins, IgG, IgM, IgA, IgD and IgE), but the amino acid sequences of the

variable regions differ quite a lot from antibody to antibody. This is because the

variable regions determine the unique shape of the antibody-binding site. The tail of

the molecule, which does not bind to antigens, is composed entirely of the constant

regions of heavy chains.

The hinge region of the antibody is a short stretch of amino acids on the heavy chain.

It provides the molecule with flexibility. This flexibility improves the efficiency with

which an antigen binds to the antibody. It can also help in cross-linking antigens into

a large lattice of antigen-antibody complexes, which are easily identified and destroyed

by macrophages.

IgG is the most common class of immunoglobulin. It is present in the largest amounts

in blood and tissue fluids. Each IgG molecule consists of the basic four-chain

immunoglobulin structuretwo identical heavy chains and two identical light chains

and carries two identical antigen-binding sites. IgG is the only class of immunoglobulin

capable of crossing the placenta; consequently, it provides some degree of immune

protection to the developing foetus. These molecules also are secreted into the

mothers milk and, once they have been ingested by an infant, can be transported into

the blood, where they confer immunity.

IgM is the first class of immunoglobulin made by B cells as they mature, and it is the

form most commonly present as the antigen receptor on the B-cell surface. When IgM

is secreted from the cells, five of the basic Y-shaped units become joined together to

make a large pentamer molecule with 10 antigen-binding sites. This large antibody

molecule is effective at attaching to antigens present on the outer coats of bacteria.

When this IgM attachment occurs, it causes agglutination.

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IgA is the main class of antibody found in many body secretions, including tears, saliva,

respiratory and intestinal secretions, and colostrum (the first milk produced by lactating

mothers). Very little IgA is present in the serum. IgA is produced by B cells located in

the mucous membranes of the body. Two molecules of IgA are joined together and

associated with a special protein that enables the newly formed IgA molecule to be

secreted across epithelial cells that line various ducts and organs. Although IgG is the

most common class of immunoglobulin, more IgA is synthesized by the body daily

than any other class of antibody.

IgD molecules are present on the surface of most, B cells early in their development,

but only a little IgD is released into the circulation. It is not clear what function IgD

performs, it is thought, it may play a role in determining whether antigens activate the

B cells.

IgE is made by a small proportion of B cells and is present in the blood in low

concentrations. Each molecule of IgE consists of one four-chain unit and so has two

antigen-binding sites, like the IgG molecule; however, each of its heavy chains has an

extra constant domain (CH4), which confers on IgE the special property of binding to

the surface of basophils and mast cells. When antigens bind to these attached IgE

molecules, the cell is stimulated to release histamines, that are involved in allergic

reactions. IgE antibodies also help to protect against parasitic infections.

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A diagram to show the 5 classes of immunoglobulins

A table to show the comparison between the innate and acquired


immune responses

Humoral Response Cell-Mediated Response


Self / Non - Self Present, Reaction is against Present, reaction is against
Discrimination foreign. foreign.
Present, reaction take a few
Absent, response is
Lag Phase days (6 days
immediate.
approximately)
Limited, the same response High, the response is
Specificity is mounted to a wide variety directed only to the agents
of agents. that initiated it.
Extensive, and resulting in
Limited hence limited
Diversity a wide range of antigen
specificity.
receptors.
Absent, subsequent Present, subsequent
exposures to agent exposures to the same
Memory
generates the same agent induce an amplified
response. response.
Antibodies produced by B
T lymphocytes recognise
Cellular Microbial lymphocytes, recognise
antigens produced by
Recognition extracellular microbial
intercellular microbes.
antigens.
Antibodies are able to
recognise many different
T cells recognise only
Recognition types of molecules such as
protein antigens.
proteins, carbohydrates and
lipids.

Good personal hygiene and washing hands removes harmful pathogens by reducing

contact transmission. Thoroughly cooking all food kills harmful pathogens. Storing

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food below 4OC prevents harmful pathogenic growth. Using separate utensils and

equipment for raw and cooked foods will prevent contact transmission. Cleaning

surfaces will kill harmful pathogens and further reduce contact transmission.

As malaria is a disease transmitted by a vector (mosquito) the use of Insect nets

covering doors, windows and surrounding sleeping areas will provide a barrier

between the mosquito and the host, as such the mosquito cannot bite the host and

transfer the pathogen.

Over time, bacteria can become resistant to certain antibiotics. This is an example of

natural selection. In a large population of bacteria, there may be some that are not

affected by the antibiotic. These survive and reproduce, creating more bacteria that

are not affected by the antibiotic. MRSA for example is methicillin-resistant

Staphylococcus aureus. It is very dangerous because it is resistant to most antibiotics.

To slow down or stop the development of other strains of resistant bacteria, people

should always avoid the unnecessary use of antibiotics and always complete the full

course. By 1955, 13% of common Staphylococcus aureus infections were resistant

to penicillin, and by 1988 this percentage was up to 91%. Center for Food Safety.

(2011) Today, penicillin is no longer recommended as the first line of treatment of

Staphylococcus infections because it is effective in less than 10% of new cases. Mayo

Clinic staff. (2011)

Tuberculosis or TB for short, is a disease caused by a bacterium called Mycobacterium

tuberculosis. Most people who are infected do not show any symptoms. But about 10

per cent go on to develop serious symptoms including shortness of breath, coughing,

fever, and even death. Infected people without symptoms are usually given a course

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of one antibiotic. Those who show symptoms need a course of several antibiotics at

once. This is to reduce the chance of strains of antibiotic-resistant bacteria emerging.

The main steps in the development of resistance are, random changes or mutations

that occur in the genes of individual bacterial cells. Some mutations protect the

bacterial cell from the effects of the antibiotic. Bacteria without the mutation die or

cannot reproduce with the antibiotic present. The resistant bacteria are able to

reproduce with less competition from normal bacterial strains.

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A diagram to show how antibiotic resistance spreads

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