Communicable Diseases Flashcards

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1
Q

What is a pathogen?

A

A microorganism that causes disease.

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2
Q

Give a brief description how bacteria cause disease

A

Their presence can cause disease by damaging cells or by releasing waste products or toxins. These toxins break down cell membranes or inactivate enzymes or prevent cell divison. In plants they often live in the vascular tissues and cause blackening and death of tissues. Eg. ring rot

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3
Q

Explain a fungal infection in relation to animals

A

Fungus lives in the skin where its hyphae (forms a mycelium) grows under the skin. It sends out reproductive hyphae which grow to surface of the skin to release spores. Redness and irriation.

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4
Q

Explain a fungal infection in relation to a plant

A
  1. Fungus lives in the vascular tissue (gains nutrients).
  2. The hypae release extracellular enzymes (cellulases) to digest the surrounding tissue causes decay.
  3. Leaves become mottled in colour, curl up and shrivel before dying.
  4. Fruit and storage organs turn black and decay.
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5
Q

Explain how viruses infect cells

A

Viruses invade cells and take over the genetic machinery and other organelles of the cell. They then cause the cell to manufacture more copies of the virus (by inserting a section of their RNA into the DNA). The host eventually bursts releasing many new viruses which will infect healthy cells.

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6
Q

Explain how protoctista causes disease with example

A

Protoctista enter the host cell and feeding on the contents as they grow. Malrial parasite is called Plasmodium (immature forms that feed on haemoglobin)

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7
Q

Discuss the differences between bacteria, fungi, viruses and protoctista

A
Domain 
- prokaryote 
- eukaryote 
- no domain 
- eukaryote
Kingdom - their names
Autotrophic/heterotrophic
- some are auto 
- hetero
- none
- some are auto
Plasmids 
- yes 
- yes 
- no 
Nucleus 
- no 
- yes 
- no 
- yes
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8
Q

Name some bacterial diseases with their characteristics

A

TB
-kills cells and tissues in many parts but lungs are most affected
Bacterial Meningitis
-infection of the meninges (membrane around brain and spinal cord) membranes become swollen and causes damge to brain and nerves
Ring Rot
-ring of decay in the vasular tissue of a potato tuber or tomato + leaf wilting

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9
Q

Name some viral diseases with their characteristics

A

HIV/AIDS
- attacks cells in the immune system and compromises it
Influenza
- attacks respiratory system and causes muscle pain and headaches
Tobacco mosaic virus
- causes mottling and discolouration of leaves

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10
Q

Name some fungal diseases with their characteristics

A

Black sigatoka
- causes leaf spots on banana plants reducing yield
Ring worm
- growth of fungus in skin with spore cases erupting through skin to cause rash (cattle)
Athlete’s foot
- growth under skin of feet (toes)

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11
Q

Name some protoctistan diseases with their characteristics

A

Blight
- affects both leaves and potato tubers (tomatoes and potatoes)
Malaria
- parasite in the blood that causes headache and fever and may progress to coma and death

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12
Q

What is the difference between passive and active defences?

A

Passive defences are present before infection; prevent the entry and spread of a pathogen. Active defences are specific chemicals in the cell walls that are produced when pathogens attack. They fortify defences already present.

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13
Q

Describe and name 4 physical plant defences

A
  1. Cellulose cell wall - acts as physical barrier and contains chemicals that can be activated when pathogen is detected
  2. Lignin thickening of the walls - waterproof and indigestable
  3. Waxy cuticles - prevent water collecting on the cell surfaces (pathogens need water to survive)
  4. Bark - has chemical defences
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14
Q

Describe and name 3 physical plant defences

A
  1. Stomatal closure - entry points, controlled by guard cells, when pathogen detected they’ll close
  2. Callose - deposited in the sieve tubes at end of growing season, blocks flow in the sieve tube, prevents pathogen spreading around plant
  3. Tylose - swelling that fills the xylem vessel, plugs the vessel so it can’t carry water, prevents spread of pathogens throughout heartwood, terpenes high conc are toxic to pathogens
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15
Q

Describe and name 6 active plant defences

A
  1. cell walls become thickened with additional glucose
  2. deposition of callose between plant cell wall and cell membrane near pathogen, impedes cellular penetration at site of infection (strengthens cell walls and blocks plasmodesmata
  3. oxidative bursts that produce highly reactive O2 damage the cells of organisms
  4. increase in production of chemicals
  5. Necrosis - deliberate cell suicide, plant can limit the pathogens access to water and nutrients (stops spread), intracellular enzymes activated by injury, destroy damaged cells and produce brown spots on leaves
  6. Canker - sunken necrotic leison in the woody tissue (main stem) causes death of cambium tissue in bark
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16
Q

Name and describe 3 chemicals used in active plant defence

A
  1. Terpenoids - anti bacterial, fungal oils (scent)
  2. Defensive proteins defensins - small cysteine rich proteins, anti microbial activity, inhibit the action of ion transport channels
  3. Hydrolytic enzymes - spaces between cells
    Chitinases (break down fungi chitin)
    Glucanases (hydrolyse glycocidic bond in glucans)
    Lysozymes (degrading bacterial cell walls)
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17
Q

Name and describe 2 chemicals used in active plant defence

A
  1. Phenols - antibiotic/fungal, tannins in bark inhibit attack of insects - bind to salivary proteins and digest trypsin and chymotrypsin, these insects don’t grow
  2. Alkaloids - caffein, nicotine, cocaine, morphine, solanine. Bitter taste. Inhibit or activiating enzyme action. Inhibit protein synthesis. Less larger animals feeding means less damage allowing pathogens in.
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18
Q

Give examples of direct transmission - direct contact in animals

A
- kissing and bodily fluids 
bacterial meningitis, HIV 
- direct skin to skin contact 
ringworm 
- microoragnisms from faeces 
diarrhoeal disease
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19
Q

Give examples of direct transmission - inoculation in animals

A
- break the skin 
HIV/AIDS 
- animal bite 
rabies 
- puncture wounds or sharing needles 
septicaemia
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20
Q

Give examples of direct transmission - ingestion in animals

A
  • contaminated food or water

amoebic dysentry

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21
Q

Give examples of indirect transmission - fomites in animals

A
  • inanimate objects like bedding, cosmetics, socks

gas gangrene, althetes foot

22
Q

Give examples of indirect transmission - droplet infection and vectors in animals

A
  • saliva, mucas expelled talking, sneezing
    influenza, TB
  • vectors transmission from animals (humans can be vectors)
23
Q

What factors affect the transmission of communicable diseases in animals?

A
  • poor diet
  • homelessness
  • overcrowded living/work spaces
  • poor ventilation
  • poor health (compromised immune system)
  • poor waste disposal
  • culture
  • socio economic
24
Q

Give examples of indirect transmission - soil contamination in plants

A

Infected plant leaves pathogen or reproductive spores in the soil so will infect next crop.

25
Q

Give examples of indirect transmission - vectors in plants

A
  • wind
  • water spores swim in surface water
  • animals feeding birds and insects; inoculation from aphids
  • humans hands, clothing, fomites, tools, farming practises
26
Q

What factors affect the transmission of communicable diseases in plants?

A
  • overcrowding
  • poor mineral nutrition reduces resistance of plants
  • climate change, increased rainfall, vectors move
  • damp, warm conditions increase survival, spread of pathogen
  • some varities are more/less susceptible
27
Q

How would you prevent the spread of disease in animals?

A
  • hand washing removes pathogens
  • improvements in living and working conditions
  • disposal of both bodily and household waste
28
Q

How would you prevent the spread of disease in plants?

A
  • leave plenty of room between plants to minimise spread
  • clear fields throughly as possible
  • rotate crops, pathogen will die without host plant
  • follow strict hygiene
  • control insect vectors
29
Q

How can pathogens penetrate the exterior defenses of plants?

A
  • mechanical wounds allow microbial entry
  • use sharp mouth parts to get through cell walls
  • form tumours on roots
  • bacteria on leaf increases risk of frost damage
30
Q

What is callose made from?

A

A carbohydrate made of B glucose monomers attached with 1-3 glycosidic bonds (sometimes 1-6) forming helical structures.

31
Q

Describe how the plant response to a pathogen attack is triggered

A

Receptors respond to molecules from pathogens or to chemicals produced by the plant cell wall when it is attacked. These attach to receptors, stimulating the release of signalling molecules to switch on genes in the nucleus, triggering cellular responses.

32
Q

Describe the primary defence of the skin

A

The skin acts as a physical barrier and prevents the entry of pathogens.
- epidermis consists of a layer of keratinocytes
Produced by mitosis, then mitigate to the surface, the cytoplasm is replaced with keratin. Called keritinisation. The dead cells shed off.
- produces sebum, inhibits growth of bacteria by lowering the pH
- sweat and tears contain lysozymes

33
Q

Describe the primary defence of blood clotting with reference to skin repair

A

Damage to the skin leaves the body open to infection. Blood clotting is used to prevent more loss of blood and to seal to prevent infection.
The enzyme cascade is activated to form the clot.
Clot formed, it drys out and scab is formed. It shrinks drwing the sides of a cut together, temporary seal while the skin gets repaired.
- deposit fibrous collagen under scab
- stem cells divide by mitosis then go to the edges to differentiate into skin
- new blood vessels grow to supply oxygen/nutrients to the new tissue
- new skin formed by contracting, scab released

34
Q

Give some words involved in the the blood clotting/enzyme cascade

A
Damaged tissue activates platelets 
Release of thromboplastin 
Catalysts prothrombin 
Ca2+ 
Leads to thrombin 
With fibrinogen 
Catalyses fibrin 
Forms a clot
35
Q

Describe the primary defence of mucous membranes

A

Airways, lungs and digestive system are at risk of infection.
The epithelial layer contains mucus secreting cells goblet cells, and mucus secreting glands.
- The mucus traps pathogens
- cilia move in a coodinated way to waft the mucus along, to the top of the trachea then is swallowed, killed in the acidiity of the stomach (lysozyme)

36
Q

Explain why we cough and sneeze

A

Areas prone to attack will respond to irritation by the pathogen or the toxins they release. The reflexes are coughing, sneezing and vomiting. The sudden explusion of air carries microorganisms

37
Q

Describe the primary defence of inflammation

A

Mast cells detect microorganisms and release a cell signalling histamine, which causes vasodilation and make the capillary walls more permeable to white blood cells and some proteins.

  • blood plasma, phagocytic white blood cells enter the tissue fluid = increased production which causes oedema
  • excess tissue fluid drained lymphatic system, initiate specific immune response, lymphocytes
38
Q

What are some other primary defences?

A
  • eyes are protected by antibodies and enzymes in tear fluid (lysozymes)
  • ear canal is lined by wax
  • mucus plug in cervix and maintain acidic conditions in vagina
39
Q

What are antigens?

A

When pathogen enters, it is recognised as forgein by the chemical markers on outer layer. They are proteins or glycoproteins. Specific.

40
Q

What are opsosins?

A

Protein molecules that attach to the antigens on the surface of pathogen. A type of antibody. Some are not specific. It enhaces the ability of the phagocytic cells to bind and engulf the pathogen.

41
Q

Describe neutrophils

A

Most common are neutrophils. Multi lobed. Manufactured in the bone marrow. Short lived, released in large numbers. Contain large amount of lysosomes. Die soon after digesting

42
Q

Explain the stages of phagocytosis

A
  1. pathogen recognised as foreign as it releases chemicals so neutrophils are attracted, chemotaxis
  2. surface of pathogen becomes coated with opsonins
  3. neutrophils bind to the opsonin attached to the antigen off the pathogen
  4. pathogen is engulfed by endocytosis forming a phagosome
  5. lysosomes fuse to the phagosome and release lytic enzymes into it
  6. release of HCl, H2O2, free radicals into the phagosome
  7. after digestion the prodcuts are absorbed into the cell
43
Q

Describe macrophages

A
  • made in bone marrow
  • travel in blood as monocytes before settling in the body tissues
  • found in lymph nodes where they mature into macrophages
  • macrophages initiates specific response
  • when it engulfs a pathogen it doesn’t fully ingest it (the antigen is saved and moved to protein complex on surface
  • it becomes an antigen-presenting cell (this increases the chances of T and B cells coming into contact with them)
  • exposes antigen so other immune cells can recognise the antigen (special protein complex ensures it isn’t mistaken for a foreign cell)
44
Q

Explain active immunity

A
  1. Requires exposure to antigen
  2. antigen invades body
  3. lag phase before protection develops
  4. long term protection
  5. memory cells produced
    Natural = infection
    Artificial = vaccination
45
Q

Explain passive immunity

A
  1. no exposure to Ag
  2. antigens given through another source
  3. immediate protection
  4. short term protection
  5. no memory cells produced
    Natural = transfer of maternal Ag to baby via milk and placenta
    Artificial = admin of pre-formed Ab’s
46
Q

List the cells that T lymphocytes develop or differentiate into

A
  • T helper cells: release cytokines that stimulate the B cells to develop and phagocytosis
  • T killer cells: attack and kill host body cells that display foreign
  • T memory cells: provide long term immunity
  • T regulator cells: shut down immune response after pathogen has been successfully removed (prevent autoimmunity)
47
Q

List the cells that B lymphocytes develop into

A
  • Plasma cells: circulate in the blood, manufacturing and releasing antibodies
  • B memory cells: remain in the body for a number of years act as memory
48
Q

Describe cell signalling

A
  • the communication is achieved via release of cytokines
  • target cell: receptor complementary to shape of signalling molecule
    1. macrophages = release monokines, some attract neutrophils by chemotaxis and others stimulate B cells to differentiate and release antibodies
    2. T cells = release interleukins, stimulate the clonal expansion and differentiation of B and T cells
    3. Interferon = inhibits virus replication and stimulates the activity of T killer cells
49
Q

Draw and label the structure of an anti body

A

Consists of 4 polypeptide chains.
Light polypeptide chain
Heavy polypeptide chain
Hinge region = allows flexibility so can grip to more than one antigen
Disulfide bridge
Variable region = shape specific to shape of antigen
Constant region = same in all antibodies, have a site for easy binding for phagocytic cells

50
Q

Explain how opsonins work

A

Opsonins = a group of antibodies that bind to the antigens on a pathogen, act as binding sites for phagocytic cells so can more easily bind and destroy the pathogen

  • some aren’t specific and stick to types of molecules that are not found in the host cells (peptidoglycan)
  • some bind to specific antigens, e.g. the pathogen might use it to bind to host cell, so opsonins binding renders antigen useless, called neutralisation.
  • assists in phagocytosis
  • prevents pathogen enters host cell
51
Q

List features associated with protein synthesis in specialised cells

A
  • numerous ribosomes
  • a lot of RER
  • a lot of golgi apparatus
  • numerous mitochondria