✨Module 4: Communicable disease Flashcards

(76 cards)

1
Q

Name 4 groups of pathogen I need to know.

A

Bacteria - TB, ring rot in potatoes and tomatoes.
Fungi - black sigatoka (bananas), athlete’s foot (human).
Protoctista - malaria, potato blight.
Virus - HIV/AIDS (human), influenza (animal), Tobacco Mosaic Virus (plant).

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2
Q

What is a vector?

A

Carries pathogens from one organism to another.

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3
Q

What are protoctista?

A

Small eukaryotic organisms that are usually unicellular. Some are parasitic (feeds off a host cell), and some of those may need a vector to transfer them to hosts.

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4
Q

How do bacteria cause disease?

A

Produce toxins that damage host cells. Breaking down their cell membranes, interfere with host cell’s genetic material so they can’t divide.

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5
Q

Describe the structure of a virus.

A

Genetic material (DNA/RNA) surrounded by a protein coat called a capsid.

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6
Q

Why are viruses the ultimate parasite?

A

Only active inside host cell, have little structure and take over whole host cell.

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7
Q

What are fungi? How can some fungi cause death of plants?

A

Eukaryotic organisms that don’t photosynthesise. They digest food extracellularly and absorb nutrients after.
Fungal infections often effect leaves of plants so they can’t photosynthesise, quickly killing the plant.
Fungi digest living cells and destroy them.
Fungi release spores that infect the body.

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8
Q

Many fungi are …

A

Saprotrophs - feed on dead and decaying matter.

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9
Q

What is the difference between a virus and a bacterium?

A

Viruses are smaller and simpler than bacteria, they can only reproduce by invading host cells and using their cellular machinery. Bacteria are single-celled organisms that can reproduce on their own.

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10
Q

Ringrot in potatoes/tomatoes.

A

Caused by gram + bacteria. Damages leaves and fruit.
Spread by insects (vector), contaminated tools, planting infected seeds.
No cure. Once infects a field, it cannot be used to grow potatoes for at least 2 years.

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11
Q

Tobacco mosaic virus.

A

Infects various plant species and damages leaves. Overcrowding or contaminated tools.
It contains ssRNA, which is directly transcribed by host cell to assemble new virions. Virions enter other cells via plasmodesmata then enter xylem and phloem. This causes stunted growth too.
No cure, but there are resistant crops.

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12
Q

Potato blight.

A

Caused by a protist. Mainly transmitted via spores through rain and wind.
No cure but resistant strains and careful management can reduce the risk.

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13
Q

Black sigatoka in bananas.

A

Fungus destroys leaves - hyphae penetrate and digest cells, turning leaves black.
Spores transmitted via rain and wind. Resistant strains are being developed, fungicide kills fungi.

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14
Q

Mycobacterium Tuberculosis.

A

Bacterial disease in humans, cows, badgers. TB damages and destroys lung tissue and suppresses immune system, so body is less able to fight off other diseases. TB bacteria target epithelial cells.
Droplet inhalation and touching surfaces.
Curable with antibiotics and vaccination.

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15
Q

How does tuberculosis cause disease?

A
  1. Triggers inflammatory response by infecting phagocytes in lungs.
  2. Infected phagocytes are sealed in coated tubercles so bacteria remain dormant.
  3. If another factor weakens immune system, bacteria become active and destroy lung tissue.
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16
Q

HIV - Human immunodeficiency virus.
AIDS - Acquired immunodeficiency virus.

A

HIV targets and replicates inside helper T cells first. This leads to AIDS, where the immune system becomes progressively weaker due to depletion of immune cells.
HIV can lie dormant in the body for many years.
HIV is a retrovirus - have the ability to make DNA in the host cell from RNA as it contains the enzyme reverse transcriptase. This DNA strand interacts with the genetic material of the host cell.
HIV is transmitted through certain body fluids such as blood, semen. Unprotected sex, sharing needles by intravenous drug users, breastfeeding.
No vaccine or cure, but anti-retro viral drugs slow the progression of the disease.

HIV has a high mutation rate. The antigens on HIV viruses can change rapidly, meaning that memory cells cannot recognise them and the body’s humoral immunity is ineffective.

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17
Q

How does HIV result in symptoms of AIDS?

A
  1. Attachment proteins bind to complementary CD4 receptor on T helper cells.
  2. HIV particles replicate inside T helper cells, killing them.
  3. AIDS develops when there are too few T helper cells for the immune system to function, so can’t destroy other pathogens.
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18
Q

Malaria.

A

Caused by Plasmodium protist and spread through bites of infected female anopheles mosquito. They act as a vector by transferring Plasmodium parasite to another organism during feeding. The parasite reproduces asexually inside the female mosquito. The female needs to take two blood meals to provide protein to lay her eggs, this is when plasmodium parasite is passed to people. It invades red blood cells, liver, brain.
Malaria is usually only common in tropical regions which have the hot and humid climates necessary for mosquitoes to breed. Thus, malaria is considered to be endemic to this region.
Currently two vaccines and preventative measures can be effective. Anopheles mosquito can be destroyed by insecticides. Mosquito nets and door screens can prevent them biting people. 虫よけスプレー
Anti malarial drugs.

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19
Q

Athlete’s foot.

A

Human fungal disease that grows and digests on warm, most skin between the toes. Causes cracking and itchy.
Anti-fungal creams are effective cure.

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20
Q

Define endemic, epidemic, pandemic.

A

Endemic - a disease that is always present in a population (even if very low numbers).

Epidemic - there is a large increase in the number of cases in a population (an outbreak).

Pandemic - an epidemic occurs on a large scale and crosses international boundaries.

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21
Q

Communicable pathogens transmitted directly and indirectly?

A

Directly - skin-to-skin contact like athletes foot or exchange of bodily fluids through STI, consuming contaminated food/drink, animal bite (rabies).

Indirectly - droplet infection (influenza/TB), vectors (rat fleas transmit bubonic plague).

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22
Q

Factors affecting transmission of communicable disease in humans?

A

Overcrowding, compromised immune system perhaps due to HIV, not keeping clean, climate change introduces new vectors like malaria.

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23
Q

Factors affecting transmission of communicable disease in plants?

A

Overcrowding increases contact, poor mineral nutrition reduces resistance of plants, animals carry pathogen that transfer to plants. Climate change - increased wind promote spread of disease.

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24
Q

Preventing disease in humans.

A

Regular handwashing, reduce overcrowding. Disposal of body fluids and household waste effectively.

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25
Preventing disease in plants.
Leave plenty of room to minimise spread of pathogens, washing hands and boots. Control insect vectors. Rotate crops to fight off pathogens, as spores and bacteria will eventually die off if they don't have access to host plant.
26
What are spores?
Produced by asexual reproduction and they grow into a new organism.
27
Physical and chemical defences in animals.
Physical: => Tough keratin skin prevents their entry. The skin also produces oily sebum that inhibits growth of pathogens. . => Trachea is lined with mucous membranes that secrete mucus. This traps microorganisms and contains lysozymes, which destroy bacteria and fungal cell walls. Mucus also contains phagocytes. Chemical: => Lysozymes in tears break down pathogens. => HCL acid in stomach kill bacteria.
28
Physical and chemical defences in plants.
Physical: => The invasion of pathogens stimulates deposition of callose and lignin between cell surface membrane and cell wall. Callose act as barriers by blocking sieve plates in the phloem, preventing the pathogens entering plant cells around site of infection. Lignin provides mechanical barrier against invasion of pathogen. Chemical: => Insect repellents like pine resin. => Hydrolytic enzymes such as chitinase are released to break down pathogen cell wall.
29
What are exotoxins and endotoxins?
Exotoxins are soluble proteins produced by bacteria released outside the bacteria. They can be highly toxic to the host, disrupting host cell structures or cell metabolism. Salmonella produce endotoxins. They are part of the outer cell membrane in gram-negative bacteria. They can trigger inflammation and other immune responses, such as fever, in humans.
30
Name 6 non-specific responses in humans.
Inflammation, phagocytosis, interferons, blood clotting, lysozyme action, fever.
31
Describe the process of blood clotting.
Platelets that have come in contact with damaged skin, via a cascade of events, produces fibrin. This forms a network, trapping platelets and forming a clot. Blood clotting prevents excess blood loss, the entry of pathogens and provides a barrier (scab) for wound healing to occur. Cytokines are proteins that tell the immune system make more white blood cells and fight off infection. They produce: Thromboplastin - enzyme that triggers the cascade of reactions. Serotonin - makes smooth muscle in walls of blood vessels contract, so lower supply of blood to the area.
32
What is DIC (disseminated intravascular coagulation)?
Condition where the body’s normal blood clotting processes become overactive, leading to both excessive clotting and bleeding at the same time. The body starts forming small clots throughout the bloodstream. These clots use up clotting factors and platelets. As a result, the body may start bleeding excessively because it runs out of the components needed to form proper clots. Anticoagulants/blood thinners reduce the body's ability to form blood clots. Examples include heparin and warfarin.
33
Examples of cytokines?
Interferons - produced by virus infected cells, help inhibit viral replication, activates macrophages, increases antigen presentation to T cells. Interleukins - produced by various immune cells, promotes inflammation and fever, activates T cells, encourages B cells to produce antibodies.
34
What happens once the blood clot forms?
The clot dries out, forming a hard tough scab that prevent pathogen entry. Then, epidermal cells below the scab start to grow, sealing the wound permanently, while damaged blood vessels regrow. Underneath this scab, there are stem cells that divide by mitosis to heal the wound.
35
What are expulsive reflexes?
Automatic responses that forces foreign substances from body through coughing or sneezing. As a result of an irritant.
36
What is the inflammatory response?
The immune systems response to an irritant, resulting in inflammation. Pain, redness, swelling.
37
Outline the process of inflammation.
=> Histamines and cytokines released by mast cells in injured tissue cause vasodilation (causing localised heat and redness). This increases flow of blood to infected area and the raised temp prevent pathogen reproducing. => Histamines increases permeability of blood vessels so antibodies, white blood cells leak out into the infected tissue and destroy the pathogen. => Cytokines attract white blood cells (phagocytes) to the site (carry out phagocytosis). Accumulation of dead phagocytes and pathogens forms visible pus layer.
38
Normal body temperature is ...
37 degrees C and is maintained by the hypothalamus in the brain.
39
What is a fever and why do we get fevers when we are ill?
A temporary increase in body temp. When a pathogen invades the body, cytokines stimulate your hypothalamus to increase body temp. It makes it harder for bacteria and virus to reproduce and survive. Also, the specific immune system works faster at higher temps.
40
What is a phagocyte?
Type of white blood cell produced in the bone marrow that engulfs and destroys pathogens and dead material. Three types: macrophage, neutrophil, dendritic cells.
41
Macrophage.
=> Long-lived and found in tissues. Macrophages travel in the blood as monocytes, which then develop into macrophages once they leave the blood. => Larger than neutrophils. => Macrophages can become antigen presenting cells. They carry out phagocytosis but don't destroy the pathogen completely. Instead they cut the pathogen up so they can display the antigens of the pathogen on their surface, so can be recognised by lymphocytes.
42
Neutrophils.
=> Short-lived and found in bloodstream. => Have a multi-lobed nucleus and phagosome. => Chemicals released by pathogens and by body cells under attack (e.g. histamine), attract neutrophils to the site of pathogen. This response to chemical stimuli is known as chemotaxis. => Once attached to a pathogen the cell surface membrane of a neutrophil extends out and around the pathogen, engulfing it and trapping the pathogen within a phagocytic vacuole. Known as endocytosis. => The neutrophil then secretes digestive enzymes into the vacuole. After killing and digesting the pathogens, the neutrophils die. Pus is a sign of dead neutrophils.
43
Dendritic cells.
=> Large phagocytic cells with lengthy extensions that give a large SA to interact with pathogens and lymphocytes. => Found throughout the body. => Once they have ingested foreign material they transport it to the lymph nodes.
44
Outline the process of phagocytosis.
1. Pathogens produce chemicals that attract phagocytes. 2. Phagocytes recognises pathogen as non-self and binds to it. 3. Phagocyte engulfs pathogen via endocytosis to form a phagosome. 4. Phagosome fuses with lysosome to form a phagolysosome. 5. Lysozymes break down and destroy pathogen. 6. Phagocyte absorbs the products from pathogen hydrolysis.
45
What are opsonins?
Chemicals that bind to pathogens and ‘tag’ them so they can be more easily recognised by phagocytes. Phagocytes have receptors on their cell membrane that bind to common opsonins, and then it engulfs the pathogen.
46
How else is a phagocyte adapted for efficient function?
Those that have engulfed a pathogen produce cytokines - they inform other phagocytes that the body is under attack and stimulate them to move to site of infection. Cytokines also increase body temp and stimulate specific immune system.
47
Role of antigen presenting cells?
T cells will only bind to an antigen if it is present on the surface of an antigen-presenting cell. This helps to attract other cells of the immune system to produce a specific immune response. Once the surface receptor of the T cell binds to the specific complementary antigen it becomes sensitised and starts dividing to produce a clone of cells.
48
What are lymphocytes?
=> Type of white blood cell smaller than phagocytes. => Have a large nucleus that fills most of the cell. => Produced in the bone marrow before birth. => Travels in the bloodstream.
49
B lymphocytes mature in … T lymphocytes mature in …
Bone marrow. Thymus gland.
50
What are T cells? What are the 4 types of T cells?
Type of lymphocyte that move from the bone marrow to the thymus gland where they mature. T cells are involved in CELL MEDIATED response. T helper cells, T killer cells, T memory cells, T regulator cells.
51
Describe the maturation of T-lymphocytes.
1. T lymphocytes (T cells) gain cell surface receptors called T cell receptors, which have a similar structure to antibodies and are each complementary to a different antigen. A small number of T cells have the same TCRs. These genetically identical cells are called clones. 2. T cells within each clone differentiate into different types of T cell: T helper cells and T killer cells. 3. There is a very large number of different T cells with different TCRs, allowing T cells to recognise a wide range of foreign antigens. 4. The matured T cells remain inactive until they encounter their specific antigen.
52
Describe the function of 4 types of T cells.
T helper cells: => They recognize and bind to foreign antigens on antigen-presenting cells. This binding activates the T helper cell, which then helps other immune cells respond to the pathogen. => After activation, T helper cells produce interleukins (type of cytokine) that stimulate B-lymphocytes and T killer cells to divide, stimulate macrophages to ingest pathogens, and also produces memory cells. => T helper cells have CD4 receptors on cell surface membrane. T killer cells: => Attach to foreign antigens on antigen-presenting cells. => produce perforin to kill the pathogen. T memory cells: => Replicate themselves when exposed to invading pathogen and remain in lymph nodes. It is part of immunological memory. If it meets antigen for the 2nd time, they divide rapidly and destroy the pathogen. T regulator cells: => Prevents the immune system from overreacting to harmful substances and preventing autoimmune conditions.
53
Clonal selection.
The process of matching antigens on antigen-presenting cells with the complementary antigens on B and T lymphocytes. This binding causes T cells to be activated and then undergo clonal expansion.
54
Clonal expansion.
Process after clonal selection where activated B and T cells divide by mitosis to produce clones/genetically identical daughter cells. There are now many T cells in the blood, all of which have specific roles. When same pathogen is present the 2nd time, memory cells undergo clonal expansion much more quickly.
55
What are B lymphocyte? What are the 2 types of B lymphocyte?
Type of white blood cell that makes antibodies. They develop from stem cells in bone marrow. They are involved in HUMORAL immunity. B effector/plasma cells, B memory.
56
Functions of the 2 types of B lymphocyte.
B memory - live for very long time and remember a specific antigen. B effector/plasma - antibody producing cells.
57
Describe maturation in B lymphocytes.
B lymphocytes have antibodies on their cell surface membrane. Antibodies are Y-shaped glycoproteins called immunoglobulins, which bind to a specific antigen on the pathogen that triggered an immune response. The B cell engulfs and processes the antigen to become an APC. Some B-lymphocytes after clonal expansion differentiate into plasma cells. Plasma cells secrete lots of antibody molecules into the blood, lymph or linings of the lungs. The other B cells become memory cells that remain in the blood for a long time.
58
What do antigens trigger?
An immune response, involving the production of polypeptides called antibodies.
59
Describe the structure of an antibody.
Consists of four polypeptide chains: 2 long heavy chains and 2 short light chains. They are connected by disulphide bridges. => Same constant region. Antibody uses this to bind to phagocytes. => Variable region that is unique to each antibody. This variable region is the antigen binding site of the antibody - it’s like the active site of an enzyme. => Hinge regions to create flexibility, so two or more separate antigens can bind.
60
How do antibodies defend the body?
1. The antibody of the antigen-antibody complex acts as an opsonin so the complex is easily engulfed by phagocyte. 2. Antibodies prevent pathogens from invading host cells. 3. Antibodies act as agglutinins so pathogens clump together. Prevent them spreading and more easy for phagocytes to engulf many at the same time. 4. Antibodies can act as anti-toxins, so they bind to toxins and make them less harmful.
61
What is an autoimmune disease? Give some examples of these.
When the immune system mistakenly attacks the 'self' cells in the healthy body tissue. The T regulator cells may not be working properly, or genetic history. Type 1 diabetes, rheumatoid arthritis.
62
Define immunity.
The body’s ability to recognize and defend against pathogens. Either active or passive.
63
Active immunity.
=> Acquired naturally when antigen enters the body, either through exposure to microbes or artificially through vaccinations. => Body produces memory cells and plasma cells to give the person long-term immunity.
64
Passive immunity.
=> Immune system hasn't been activated and no memory cells have been produced.
65
Different types of immunity.
Natural active immunity - exposure to pathogen. Artificial active immunity - vaccination. Artificial passive immunity - given an injection of antibodies. Natural passive immunity - antibodies received from another organism. Foetuses receive antibodies across placenta from mother, colostrum.
66
Specific and non-specific immunity.
Non-specific - what humans are born with, including barriers, like skin and stomach acid, macrophages. Specific immunity - only responds to an antigen. This relies on lymphocytes produced in bone marrow. Learned by the body based on previous exposure to pathogens.
67
What are antibiotics?
Target specific processes in bacteria, such as their ability to produce cell walls or proteins. This leads to the death of the bacteria or stops their growth and spread.
68
Widespread use of antibiotics has led to ...
Antibiotic resistance. Genetic mutations may occur in a bacteria. When the antibiotic is used, it leads to natural selection of the bacteria with the mutation (as all other bacteria without the mutation are affected), resulting in this resistant bacteria being able to reproduce greatly and pass on the mutation.
69
Reducing antibiotic resistance.
=> Doctors avoiding the overuse of antibiotics, prescribing them only when needed. Doctors should test the bacteria first to make sure it's the correct antibiotic. => Antibiotics not being used in non-serious infections that the immune system will ‘clear up’. => When prescribed a course of antibiotics, the patient finishing the entire course (even if they feel better after a few days) so that all the bacteria are killed, and none are left to mutate to become resistant strains. => Antibiotics not being used for viral infections.
70
What are personalised medicines and synthetic biology?
-> Personalised medicines are individualised to the patients DNA. As genes play a role in how a person responds to a drug, different people may have different reactions to the same type of drug. -> Synthetic biology can be used to create artificial biological compounds. It uses genetic engineering and other types of advanced technology. For example: new types of T cell receptors has been created which can specifically bind to antigens found on cancer cells. Bacteria can be reprogrammed to sense and target cancer cells at various stages of their life cycle.
71
Alternatives to treat bacterial infections?
Bacteriophages are viruses that target and kill bacteria, prebiotics and probiotics support the growth of beneficial bacteria in the gut, helping to prevent infections.
72
What are vaccines?
Vaccines are dead or weakened viruses that can be injected into an individual, in order to stimulate the immune system to develop immunological memory against the pathogen. This way, when an individual comes into contact with the live virus, the body already has an efficient mechanism in place to rapidly detect and eliminate it. Vaccines cause plasma cells to release antibodies.
73
Vaccinations rely on antigen structure staying the ...
Same. A vaccine stimulates the primary immune response, and produces memory cells against a specific antigen. It assumes that if there is a second infection, then the same antigen will be present on the pathogen.
74
Mass vaccination contributes to ...
Herd immunity. When majority of population is vaccinated against a pathogen, it breaks the pathogen’s chain of infection. This means that the virus essentially disappears because it is unable to pass from person to person. This means that members of the population, such as infants, who have not received vaccinations, are protected against the pathogen.
75
Describe the process of making monoclonal antibodies.
A mouse is injected with an antigen. The B-cells that produce the antibody are removed from the spleen and fused with a myeloma (type of cancer cell) to form a hybridoma. Each hybridoma reproduces rapidly, resulting in millions of monoclonal antibodies.
76
How are monoclonal antibodies used in cancer treatment?
Cancer cells have antigens called tumour markers. We can design monoclonal antibodies specific to these antigens, so that they can neutralise cancer cells, as well as to attract TC cells. We can also attach anti-cancer drugs to the monoclonal antibodies. Medical diagnosis – monoclonal antibodies can be used to detect particular antigens in patient samples of blood or tissue. For example, pregnancy testing uses monoclonal antibodies to detect for hCG. If a woman is pregnant, hCG will be found in urine, so we can do urine tests using monoclonal antibodies.