Module 4: Communicable Diseases Flashcards

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1
Q

Define the term pathogen

A

Pathogens are organisms that cause a disease.

  • Take nutrition from host as energy source.

Bacteria (prokaryotes) ‐ e.g. tuberculosis
Fungi e.g. athlete’s foot
Viruses e.g. HIV
Protoctista e.g. malaria

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2
Q

Describe the 4 main groups of pathogens including examples of each

A
Bacteria (Prokaryote Kingdom)
• Smaller the Eukaryote cells
• Reproduce rapidly
• Damage cells through release of toxins
• e.g. TB & Ring Rot in potatoes and tomatoes

Fungi
• Fungus often lives in skin, hyphae form a mycelium
• Reproductive hyphae grow into the skin & release spores (redness to skin)
• In plants lives in vascular tissue to gain nutrients
• Hyphae release extracellular digestive enzymes to break down cellulose. (decays plant)
• e.g. Black sigatoka, ringworm

Protoctista
• Enter host cell & feed on the contents of the cell
• Malaria parasite Plasmodium has immature forms
which feed on haemoglobin
• e.g. Potato Blight

Viruses
• Viruses invade cells and take over genetic
machinery & other organelles
• Causes the cell to manufacture more copies of the virus
• Host cell eventually bursts, releasing new viruses to
invade new host cells
• e.g. HIV, Influenza, tobacco mosaic virus

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3
Q

What are the 2 main methods of disease transfer?

A

Direct transfer:
Transmission via Physical contact, Faecal transmission,
Droplet infection, Spores transmission

Indirect transfer:
Transmission via vectors e.g. malaria via female anopheles mosquitos and Dutch elm disease is caused by a beetle vector.

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4
Q

What factors affect disease transfer?

A
Poor diet
Poor health
Overcrowding
Migration
Poor ventilation
Sex
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5
Q

Explain disease transfer in plants

A

Can be spread directly or indirectly. Most common infection of plants is through the roots, particularly if there is any damage around the roots.
This is an example of direct transmission.

Airborne transmission ‐ Fungi releasing spores which get carried by the wind.

Once a pathogen has infected it may infect all vascular tissue, when the leaves are shed the pathogen will be spread to the soil where it can infect other plants.

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6
Q

What are the 2 main types of plant defences?

A
Physical defences (active or passive)
Chemical defences
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7
Q

Why do plants have defences?

A

As plant provide a rich source of nutrients for many organisms they need to have defences in order to protect themselves. Plants do not have an immune system so they require defences in order to prevent extensive damage.

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8
Q

What are passive defences?

A

Passive defences are defences present prior to infection, their role is to prevent spread and infection of the pathogen. They can be split into physical and chemical defences.

Examples:
Cellulose Cell Wall ‐ Physical barrier waterproofed by lignin, contains tannins ‐ chemical defences which are activated if a pathogen is detected.

Waxy Cuticle ‐ Prevents water collecting which can contain pathogens.

Bark ‐ Physical barrier, contains chemicals which will work against pathogens.

Tylose formation ‐ Tylose is a balloon like projection which fills the xylem, acts a plug preventing the xylem from carrying water, prevents the spread of pathogens. Tylose contains high levels of terpenes which are toxic to many pathogens.

Callose ‐ Callose is a large polysaccharide molecule which is deposited within sieve tubes when a pathogen is detected. It blocks the flow in the sieve tube and at plasmodesmata preventing the spread of the pathogen into cells.

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9
Q

What are chemical defences?

A

Terpenoids, Phenols, Alkaloids, and hydrolytic enzymes can be found in plant tissues which have anti‐pathogenic properties.

Tyloses and tannins are found in bark before infection, however they use a lot of energy to create many chemicals which are not made until infection is detected.

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10
Q

What are active defences?

A

When a plant becomes infected with a pathogen, proteins in the cell wall of the plant detect and they plant can respond:

These include‐
• Cellulose cell walls thicken with more cellulose
• Callose deposition
• Oxidative bursts that produce highly reactive oxygen molecules ‐damage the pathogen
• Necrosis ‐ deliberate death of infected cells to stop spread
• Increase in the production of chemicals (terpenoids, phenols, alkaloids, defensins, hydrolytic enzymes)

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11
Q

What are primary defences?

A

Defences that prevent a pathogen from entering the body.

E.g.

  • Lysozyme in tears- kills pathogens in the eyes.
  • Mucus traps pathogens in airways.
  • Blood clots prevents pathogens entering the blood.
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12
Q

Describe primary defences and outline their importance

A

1) Mucous membranes- specialised epithelial tissue covered in mucous:
At exchange surfaces, the diffusion distances into the blood are small ‐ this makes them more susceptible to infection from pathogens. Mucous membranes can coat these surfaces as a primary defence.

2) Coughing, sneezing and vomiting:
Coughing, sneezing and vomiting are expulsive reflexes ‐ the irritation caused by microbes or their toxins causes the expulsion which will carry microbes with it .

3) Inflammation- swelling and redness of tissue caused by infection:
• Microbes detected by mast cells which release histamine.
• Histamine causes vasodilation ‐ makes capillaries more permeable so more WBCs can leave.
• More tissue fluid forms because more plasma leaves.
• This causes swelling (oedema).
• Tissue fluid can drain into the lymph vessels so that pathogens may come into contact with lymphocytes (WBCs) and cause a specific immune response.

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13
Q

Describe how the blood clots

A

• Damage to a blood vessel ‐ platelets bind to exposed collagen to form a temporary platelet plug.
• Platelets also release clotting factors which activate an enzyme cascade.
• Enzymes cause fibrinogen to form insoluble fibres which attach to the plug.
• RBCs are also trapped ‐ this forms a clot.
• Clot dries and forms a scab which pulls the skin closer together.
• Under the skin collagen is deposited.
• Stem cells in epidermis divide by mitosis and differentiate to form new skin cells at the
edge of the cut.
• New blood vessels form.
• When edges of the cut are drawn together the repair is complete.

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14
Q

Define a secondary defence

A

Secondary defences attempt to kill a pathogen after it has entered the body.

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15
Q

What is a phagocyte?

A

Phagocytes attempt to kill pathogens before they can reproduce and cause any symptoms ‐ they are non‐specific.

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16
Q

Describe the 3 types of phagocyte

A

• Neutrophils:
‐ most common
‐ travel in blood
‐ pass into tissue fluid (possible because they can change shape and have a multilobed nucleus, allowing them to fit between gaps in endothelium)

• Macrophages:
‐ larger
‐ travel in blood as monocytes
‐ settle in lymph nodes and become macrophages
‐ initiate immune response (antibody production)

• Antigen Presenting Cells:
‐ when in contact with antigens can mount a full immune response
‐ activates T & B Lymphocytes (clonal selection)
‐ cells signal using hormone like chemicals (cytokines)
‐ stimulates production of B & T cells and Macrophage

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17
Q

How does a phagocyte engulf and digest a pathogen?

A
  1. receptor on phagocyte’s cell surface membrane binds to antigen on pathogen’s cell surface membrane.
  2. pathogen engulfed by endocytosis.
  3. this produces a phagosome (phagocytic vesicle).
  4. lysosomes fuse with phagosome, releasing enzymes (lysins) into it.
  5. the pathogen is digested into amino acids and fatty acids etc.
  6. products are absorbed into cytoplasm by diffusion.

The whole series of events is co ordinated by hormone like chemicals knows as cytokines. Cytokines stimulate B cells, T cells and Macrophages.

18
Q

What are B and T lymphocytes?

A

White blood cells are made in the bone marrow when cells differentiate into phagocytes and lymphocytes.

  • B lymphocytes mature in the bone marrow
  • T lymphocytes mature in the thymus

Both are cells with large nuclei and specialised receptors on their cell surface membranes.

Mature B and T lymphocytes circulate around the blood and lymph.

19
Q

Triggering an immune response

A

• The antigens on the pathogen’s surface communicate to our body’s cells that it is foreign.

• To initiate an immune response, the pathogens have to be detected by B and T lymphocytes with the correct complementary receptors to the pathogen’s antigens. The
white blood cells communicate using signalling molecules called interleukins.

  • Infected cells sometimes get the pathogen’s antigens on their surfaces ‐ this helps to select the right B and T lymphocytes.
  • Macrophages in the lymph nodes engulf and digest pathogens. They separate the pathogen’s antigens and incorporate them into their own cell surface membrane. They are now antigen presenting cells ‐ they increase the chances of the correct T lymphocytes locating the foreign antigens.
  • The selection of the correct lymphocytes with receptors complementary in shape to the antigens is call clonal selection.
  • More of these lymphocytes are needed to fight the pathogens so they divide by mitosis in clonal expansion.
20
Q

Describe 3 examples of cell signalling in the immune response

A
  • Pathogens antigens communicate to body cells that they are foreign.
  • Infected with foreign antigens on surface communicate to lymphocytes to be selected in clonal selection and to T killer cells that they need to be killed.
  • Macrophages engulf and digest pathogens and incorporate the pathogen’s antigens on their cell surface membrane ‐ communicates to T lymphocytes to be selected in clonal selection.
  • T helper cells release cytokines ‐ bind to receptors on B cells and stimulate them divide by mitosis and differentiate.
21
Q

The changes and roles of T lymphocytes in the immune response

A
  • Differentiate into 4 types of cell
  • T helper cells (T h) release cytokines with specific shapes which bind to complementary receptors on the cell surface membrane of B lymphyocytes, stimulating them to divide by mitosis and differentiate. They also stimulate macrophages to carry out more phagocytosis.
  • T killer cells (T k) search for and kill infected host cells by secreting protease enzymes into them.

• T memory cells (T m) which stay in the blood in case there is a second invasion by the same pathogen. They allow a faster secondary response because they recognise the antigen and can make clones and change to form new T cells more quickly than in the primary
response.

• T regulator cells (T r) shut down the immune response once the pathogen has been removed

22
Q

The changes and roles of B lymphocytes in the immune response

A
  • Differentiate into two types of cells involved in the humoral response :
  • Plasma cells which produce and secrete antibodies which are complementary in shape to the antigen.
  • B memory cells which stay in the blood in case there is a second invasion by the same pathogen. They allow a faster secondary response because they recognise the antigen and can make clones and change to form new plasma cells and so antibodies are made more quickly than in the primary response.
23
Q

Define antigens and antibodies

A

Antigens ‐ protein/glycoprotein found on the cell surface membrane of cells. Foreign antigens stimulate an immune response.

Antibodies ‐ proteins which identify and neutralise antigens. Each antibodies is specific to a particular antigen due to the complementary shapes of the antigen and variable region of the antibody.

  • Antibodies are made by B lymphocytes
  • They are released in response to infection
  • 1 specific antibody per antigen
24
Q

Describe how the structure of antibodies are related to their function

A

4 polypeptide chains held together by disulphide bonds‐ Y
shaped molecule.

Constant region - for binding to phagocytes

Variable region - for binding to antigens

More than one variable region - allows attachment to more than one antigen (hence attaching to more than one pathogen)

Hinge region - Allows flexibility for the branches of the Y shaped molecule to move closer/further apart to bind to more than one antigen

25
Q

The function of antibodies

A
  • antibodies bind to antigens on pathogen
  • neutralisation of pathogens…
  • antibodies cover binding sites on pathogen
  • which prevents their entry to host cell agglutination of pathogens…
  • multiple variable regions allows antibodies to clump/bind together many pathogens
  • clump too large to enter host cell and increases likelihood of being consumed by (named) phagocyte
26
Q

What is the role of opsonins?

A

A group of antibodies that bind to antigens, act as a binding site for phagocytes so as the pathogen can be destroyed.

Some opsonins are specific to antigens, some just bind to molecules not found in the host e.g. peptidoglycan cell walls (cell walls of prokaryotes).

An antigen on the pathogen can sometimes be used as a binding site to the host cell so if the opsonin binds here this is known as neutralisation.

27
Q

What is the role of antitoxins?

A

Antibodies which are able to bind to toxins produced by the pathogen which renders them harmless.

28
Q

Compare and contrast the primary and secondary immune responses?

A

Primary:
• there is a time delay to trigger immune response after first infection
• no memory cells ‐ slow antibody production and few produced

Secondary:
• T memory cells & B Memory Cells are already present in the blood ‐ antibody production is immediate
• higher level of antibody production and antibodies produced more quickly

B Memory Cell & T memory cells ‐ remain in the blood for a long period of time acting as immunological memory.

29
Q

What is an autoimmune disease?

A

This is when the immune system attacks the body. An autoimmune disease occurs when our antibodies begin to attack our own antigens. The cause of this is unknown.

E.g. Arthritis ‐ Antibodies attack the membranes around joints.
Lupus ‐ Antibodies attack proteins in the nucleus.

30
Q

Why do we need to find new drugs?

A
  • new drugs needed to combat new diseases

* new antibiotics needed as some strains of bacteria have evolved antibiotic resistance

31
Q

How do we find new drugs?

A

Antibiotics are produced naturally by microbes (the fungus Penicillium makes the antibiotic penicillin)
• discover new antibiotics

Some plants produce compounds with medicinal properties
• traditional plant medicines ‐‐> isolate the active ingredient
• cuts down time and cost (medicinal properties) It is important to maintain biodiversity
• new sources of drugs

32
Q

What are antibiotics?
In what circumstances are they useful?
In what circumstances does using antibiotics have risks?

A

Antibiotics are used to treat/ avoid bacterial infection.

  • Prevent infection after surgery ‐ reduces complications/death rate.
  • To treat infections that the body cannot ‘fight off’.

• Overuse and misuse of antibiotics allows bacterial strains to become resistant to antibiotics. This makes certain antibiotics less effective.

33
Q

How does over use of antibiotics lead to antibiotic resistance in bacteria?

A
  • During WWII, there was wide use of antibiotics to treat infections in wounds etc. This continued through the 20th century.
  • Over‐use and misuse of antibiotics leads to resistance as the bacteria are exposed to them far more.
  • Resistance is a beneficial trait so any resistant bacteria are more likely to survive and reproduce, passing on their genes to the next generation. In this way the whole species can become resistant to antibiotics.
34
Q

Explain why the term ‘immune’ is incorrect when referring to bacteria and antibiotics (2).

A
  • They are resistant

* Immune implies they have an immune system which they don’t as they are single celled organisms

35
Q

What is a vaccination?

A

A deliberate exposure to antigenic material which
activates the immune system, to make an immune response and provide immunity as a result of the
production of memory cells in the primary response to the antigenic material.

source of antigens:
• harmless/dead version of pathogen for that disease
• microbes with very similar shaped antigens
• antigens themselves

36
Q

What is the difference between epidemic and pandemic?

A

epidemic ‐ a disease that spreads quickly an affects a
large proportion of the population.

pandemic ‐ a disease which spreads worldwide over
many countries and continents.

37
Q

What is the difference between herd and ring vaccination?

A

There are two ways governments go about vaccinating people to control a disease.

• Herd vaccination:
> vaccinate all people at risk
> stops infection spreading

• Ring vaccination:
> requires people to report victims
> vaccinate all people living with or near victim
> contains spread within ring

38
Q

Why do some people chose not to get immunised even though this is the advice given to them by the government?

A
  • too busy/can’t be bothered to go to the doctors
  • media scare stories
  • concerned about side effects
  • allergic to vaccine
  • fear of needles
  • religious reasons
  • cost of vaccine is too expensive
39
Q

Why do governments want people to be vaccinated aside from the direct health benefits?

A
  • prevention of disease can save days lost at work by many people ‐ which could harm the economy
  • it costs less to immunise many people than it would to treat them
  • the health service may not be able to cope if large numbers of people became infected
40
Q

Why are the elderly (and others) encouraged to get a vaccine for the influenza virus every year?

A
  • vaccine is changed every year
  • as there are different strains of the virus each year as it has mutated from the previous year
  • new strains have different antigens
  • the old antibodies from the previous year aren’t complementary to the new antigen and the new vaccination will encourage the new antibodies to be made
41
Q

Compare and contrast, active, passive, natural and artificial immunity

A

Natural immunity is gained in the normal course of living.

Artificial immunity is gained by a deliberate exposure to antibodies or antigens.

Natural and artificial immunity can be passive or active.

Passive immunity ‐ acquired without the activation of the lymphocytes ‐ provided by antibodies that have not been made by the person’s own immune system.

Active immunity ‐ acquired by the activation of the person’s own immune system