4.1.1 communicable diseases, disease prevention and the immune system Flashcards

1
Q

What is bacteria as a pathogen?

A

They are prokaryotic cells with no membrane-bound organelles.

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2
Q

How can bacteria be classified?

A

By their cell shape or their cell walls.

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3
Q

What do bacteria cell walls determine?

A

The cell wall determines the antibiotics used.
Gram-positive=purple stain e.g. MRSA.
Gram-negative=pink/red stain e.g. E.coli.

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4
Q

What are viruses?

A

A short section of RNA surrounded by protein.
They infect cells by inserting own RNA into cell DNA=> cell produces more.

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5
Q

How do viruses affect the body?

A

Takes over metabolism and, material inserted and replicated.

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5
Q

What are bacteriophages and how do they infect?

A

Viruses which infect bacteria.
-They attach to host cell
-Insertion of viral nucleic acid
-Replication
-Synthesis of viral proteins from nucleic acids
-Assembly of virus particles
-Lysis of host cells

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6
Q

How does bacteria affect the body?

A

Produce toxins which destroy membranes.

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7
Q

How does Protista affect the body?

A

Takes over cells and digests insides.

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8
Q

How does fungi affect the body?

A

Digests and destroys living cells.

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9
Q

What are Protoctista/Protista?

A

Eukaryotic cells-singular/multi-cellular.
They often require a vector (infections but not infected).

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10
Q

What is fungi?

A

Eukaryotic cells-singular/multi-cellular.
Saprophytes-feed off of dead decaying matter.
Prevent photosynthesis and produce spores and infect others.

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11
Q

What are some examples of bacterial diseases?

A

Bacterial Meningitis:
symptoms=rash and fever
treatment=antibiotics(early stage) and vaccines
spread=secretions(saliva)-close contact.
Tuberculosis (TB):
symptoms=night sweats, fever, suppressed immune system, weight loss.
treatment=antibiotics
prevention=vaccinations and improved living standards.
spread=droplets
Ring rot:
symptoms=discolouration, water loss, browning vascular rings, and grey-white ooze
treatment=no cure
spread=infected seeds

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12
Q

What are some examples of viruses?

A

HIV/AIDS:
symptoms=vomiting, diarrhoea, nausea, weakened immune system, swollen lymph nodes, weight loss, and fatigue.
treatment=medicine (cannot cure but helps live longer)
spread=sexual intercourse and sharing used needles.
Influenza:
symptoms=vomiting, fever, diarrhoea, headache, nausea, mucus in airways.
treatment=no cure
prevention=flu vaccine
spread=droplets from infected people.
Tobacco Mosaic Virus:
symptoms=damaged leaves, flowers, fruit, stunted growth and reduced yield.
treatment=resistant crop strains but no cure.

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13
Q

What are some examples of Protoctista?

A

Malaria:
symptoms=weakened immune system, poor appetite, and insomnia.
treatment=no vaccines
prevention=mosquito nets, and door screens.
spread=through infected female mosquitos who lay eggs and need blood to lay them.
Potato/tomato blight:
symptoms=reduced size, damages leaves, and abnormal colour (yellowing).
treatment=no cure
prevention=careful management and chemical treatment (reduce infection rate)
spread=wind or water-splash.

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14
Q

What are some examples of fungi?

A

Black Sigatoka:
symptoms=turns leaves black, streaks or leaf spots, and areas of dead leaves.
treatment=fungicide but no cure.
(bananas)
Ring-worm:
symptoms=fever, headache, red rash on groin/legs.
treatments=antifungal cream
spread=close contact and infected objects.
(cattle)
Athlete’s foot:
symptoms=itchy white patch between toes, soreness, and flaking feet.
treatment=antifungal cream
spread=infected skin scales and contact with fungi in damp areas.
(humans)

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15
Q

How can direct contact causing spread disease be prevented?

A

-hygiene (washing hands)
-cleaning and disinfected cuts/abrasions
-condoms during sexual intercourse

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16
Q

How can faecal/oral transmission be prevented?

A

-treatment of waste and drinking water
-through washing of fresh food

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17
Q

What ways can diseases be spread?

A

-Direct contact
-Faecal/oral transmission
-Droplet infection
-Spores

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18
Q

How can droplet infection be prevented?

A

-covering mouth when sneezing/coughing
-using tissue and then disposing

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19
Q

How can transmission by spores be prevented?

A

-use of a mask
-washing skin after contact with soil

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20
Q

What are examples of vectors?

A

-Wind
-Water
-Animals
-Humans

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21
Q

What factors affect the transmission of communicable diseases in plants?

A

-planting varieties of crops that are susceptible to disease.
-overcrowding increases the likelihood of contact.
-poor mineral nutrition reduces resistance of plants.
-damp, warm conditions increase the survival and spread of pathogens and spores.
-climate change.

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22
Q

How do plants use callose as a physical defence against pathogens?

A

Plants rapidly produce high levels of callose (polysacc made of beta glucose).
It is used as a barrier between cell walls and membranes.
Lignin is also added to strengthen the barrier.
Callose blocks sieve plates in phloem so seal off tube.
It is deposited in plasmodesmata preventing healthy cells from being infected.

23
Q

What are the chemical defences of plants used to defend against pathogens?

A

Insect repellents- e.g. pine resin and citronella.
Insecticides- e.g. pyrethrins act as insect neurotoxins, and caffeine which is toxic to insects and fungi.
Antibacterial compounds including antibiotics- e.g. phenols, defensins which are plant proteins that disrupt bacterial and fungal cell membranes, and lysosomes.
Antifungal compounds- e.g. phenols, caffeine, saponins, and chitinases (enzymes which break down chitin in fungal cell walls).
Anti-oomycetes- e.g. glucanases which are enzymes made by plants to break down glucans.
General toxins- e.g. cyanide.

24
Q

What are the non-specific defences which keep pathogens out the body of animals?

A

Skin: acts as a physical barrier, and produces sebum which inhibits pathogen growth.
Skin flora: natural healthy bacteria.
Mucous membranes: traps pathogens, and contains lysozymes which destroy bacterial and fungal cell walls.
Lysozymes: in tears and urine, and stomach acid.

25
Q

How does the body react to a wound (also a barrier mechanism)?

A

Platelets secrete several substances including:
Thromboplastin- enzyme that triggers a cascade of reactions resulting in a blood clot.
Serotonin- makes the smooth muscle in walls of blood vessels contract and reduce blood supply to the area.

26
Q

What is the inflammatory response?

A

It is the swelling of skin around a rupture.
Mast cells are activated when skin is ruptured. The cells release histamines and cytokines.
Cytokines attract white blood cells (signal molecules).
Histamines make blood vessels dilate causing localised heat and redness, and the high temperature prevents pathogens reproducing.
Histamines also increase permeability of blood vessel walls causing more tissue fluid to escape.

27
Q

What are the stages of phagocytosis?

A
  1. Phagocyte attracted by chemicals produced by pathogen.
  2. Phagocyte recognises pathogen as non-self and binds to it.
  3. Phagocyte engulfs the pathogen to form phagosome, lysosome moves towards phagosome and combines with it, forming phagolysosome.
  4. In phagolysosome, enzymes break down the pathogen.
  5. Digested pathogen absorbed by phagocyte, antigens combines with MHC (macrophage histocompatibility complex) in its cytoplasm.
  6. MHC/antigen complex is displayed on phagocyte membrane making an antigen presenting cell.
28
Q

What role do cytokines and opsonins have in phagocytosis?

A

Cytokines- cell-signalling molecules.
Increase body temperature and stimulate the specific immune system.
Opsonins- chemicals that bind to pathogens and ‘tag’ them so they can be more easily recognised by phagocytes.

29
Q

What are antibodies?

A

Antibodies are Y-shaped glycoproteins (immunoglobulins) which bind to a specific antigen on the pathogen or toxin.

30
Q

What is the structure of an antibody?

A

Antibodies are made up of two identical long polypeptide chains (heavy chains), and two shorter chains (light chains).
The chains are held together by disulfide bridges.
Variable region- different to different antibodies.
Constant region- same in all antibodies.

31
Q

How do antibodies defend the body?

A
  1. Antibody acts as an opsonin so complex is easily engulfed and digested.
  2. Most pathogens cannot invade host cells once part of antigen-antibody complex.
  3. Antibodies act as agglutinins causing complexes to clump together which prevents them spreading through the body.
  4. Antibodies act as anti-toxins.
32
Q

Where do B lymphocytes and T lymphocytes mature?

A

B lymphocytes= Bone marrow
T lymphocytes= Thymus gland

33
Q

What are the main types of T lymphocytes?

A

T helper cells.
T killer cells.
T memory cells.
T regulator cells.

34
Q

What are T helper cells?

A

T helper cells have CD4 receptors which bind to surface antigens on antigen-presenting cells.
They produce interleukins (a type of cytokine)-they stimulate the activity of B cells, which increases antibody production, stimulates production of other types of T cells, and attracts and stimulates macrophages to ingest pathogens with antigen-antibody complexes.

35
Q

What are T killer cells?

A

T killer cells destroy the pathogen carrying the antigen. They produce perforin which kills the pathogen by making holes in the cell membrane so it is freely permeable.

36
Q

What are T memory cells?

A

T memory cells live long and are part of the immunological memory.
If they meet an antigen a second time, they divide rapidly to form a huge number of clones of T killer cells.

37
Q

What are T regulator cells?

A

T regulator cells suppress the immune system, acting to control and regulate it.
They ensure the body recognises self-antigens and does not set up an autoimmune response.

38
Q

What are the main types of B lymphocytes?

A

Plasma cells.
B effector cells.
B memory cells.

39
Q

What are plasma cells?

A

Plasma cells produce antibodies to a particular antigen and release them into circulation.
Active plasma cells only live for a few days but produce around 2000 antibodies per secon.

40
Q

What are B effector cells?

A

B effector cells divide to form the plasma cell clones.

41
Q

What are B memory cells?

A

B memory cells live long and provide the immunological memory.
They are programmed to remember a specific antigen and enable the body to make a rapid response.

42
Q

What is cell-mediated immunity?

A
  1. In non-specific defence, macrophages engulf and digest pathogens in phagocytosis. They process the antigens from the surface of the pathogen to form antigen-presenting cells.
  2. The receptors on some of the T helper cells fit the antigens. These T helper cells become activated and produce interleukins, which stimulates more T cells to divide by mitosis. They form clones of identical activated T helper cells that all carry the right antigen to bind to a particular pathogen.
  3. The cloned T cells may: Develop into T memory cells, which gives a rapid response if the pathogen invades again.
    Produce interleukins that stimulate phagocytosis.
    Stimulate the development of a clone of T killer cells that are specific for the presented antigen and then destroy infected cells.
43
Q

What is humoral immunity

A
  1. Activated T helper cells bind to the B cell APC (clonal selection)-the point at which the B cell with the correct antibody to overcome a particular antigen is selected for cloning.
  2. Interleukins produced by the activated T helper cells activate the B cells.
  3. The activated B cell divides by mitosis to give clones of plasma cells and B memory cells (clonal expansion).
  4. Cloned plasma cells produce antibodies that fit the antigens on the surface of the pathogen, bind to the antigens and disable them, or act as opsonins or agglutinins (primary response).
  5. Some cloned B cells develop into B memory cells (seconday response).
44
Q

Which pathogens are inside and outside cells?

A

Inside:
Virus
Protist
Outside:
Bacteria
Fungi

45
Q

What is an autoimmune disease?

A

The immune system stops recognising ‘self’ cells and attacks healthy body tissue.

46
Q

What are some examples of autoimmune disease?

A

Type 1 diabetes= insulin-secreting cells of the pancreas.
treatment: insulin injections, pancreas transplants, and immunosuppressant drugs.
Rheumatoid arthritis= joints.
treatment: no cure, anti-inflammatory drugs, steroids, pain relief, and immunosuppressant drugs.
Lupus= skin, joints, can attack any organ in the body.
treatment: no cure, anti-inflammatory drugs, steroids, and immunosuppressants.

47
Q

What is natural active immunity?

A

-Normal immune response
-Active- body produces antibodies.

48
Q

What is natural passive immunity?

A

-Newborn babies rely on immunity from mothers.
-Foetus receives antibodies from placenta.
-First milk sample (colostrum) is high in antibodies.
-Passive- baby doesn’t produce antibodies itself.

49
Q

What is artificial passive immunity?

A

-Antigens produced by another organism and injecting into the bloodstream of another.
e.g. Tetanus-injections from antibodies from horses.
-short lasting immunity.

50
Q

What is artificial active immunity?

A

-vaccination.
-stimulates to produce antibodies by immune response by injecting ‘safe’ antigens.
-the antigens are not normally part of a living pathogen.

-vaccines.
-killed or inactivated bacteria and viruses.
e.g. whooping cough.
-attenuated (weakened) strains of live bacteria or viruses.
e.g. rubella and polio.
-toxin molecules have been altered and detoxified.
e.g. diphtheria and tetanus.
-isolated antigens extracted from pathogen.
e.g. influenza.
-genetically engineered antigens
e.g. hepatitis B.

51
Q

How do vaccines prevent epidemics/pandemics?

A

At the beginning of an epidemic, mass vaccination can prevent the spread of the pathogen into wider population-having to change regularly to remain effective.
Creation of herd immunity- those vaccinated give protection to those without immunity.

52
Q

What is pharmacogenetics?

A

Personalised medicine- a combination of drugs that work with your individual combination of genetic and disease.
-Involves looking at the genome of a patient and the genome of the invading pathogen before deciding how to treat them.

53
Q

What is synthetic biology?

A

Using genetic engineering to develop rare, expensive populations of bacteria to produce much needed therapeutic drugs.
-Enables the use of bacteria as biological factories.
-Nanotechnology is a strand of synthetic biology= use of tiny non-natural particles to deliver drugs to very specific sites.

54
Q

What is the issue with antibiotic resistance?

A

Antibodies interfere with the metabolism of bacteria without affecting the metabolism of human cells (selective toxicity).
-Antibodies are overused/overprescribed by Doctors= bacteria is becoming more resistant to more and more antibiotics.
Random mutations may produce a bacterium resistant to antibiotics, reproduce rapidly to grow a population of antibiotic-resistant bacteria.
e.g. MRSA and c.difficile.

55
Q

How can antibiotic-resistant infections be reduced long-term?

A

Minimising the use of antibiotics, and ensuring the full course of antibiotics is taken.
Good hygiene in hospitals, care homes, and in general.