Disease Flashcards

(44 cards)

1
Q

Virus

A

-Not alive
-Cannot reproduce outside of cell.
-Capsid with sites to attach to host cells.
-Eg tobacco mosaic virus, HIV

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2
Q

Fungus

A

-Eukaryotic
-Chitin cell wall
-Can be single or multicellular
-Eg black sigatoka, ring worm

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3
Q

Bacteria

A

-Prokaryotic.
-Peptidoglycan cell wall.
-Divide by binary fission.
-Eg Ring rot, tuberculosis

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4
Q

Protists

A

-Eukaryotic.
-Singular or multicellular.
-Eg tomato blight, malaria.

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5
Q

Direct transmission

A

-Where a pathogen is passed from one organism to another without any stages.

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6
Q

Direct contact

A

-Two organisms touching.
-Skin to skin.
-Exchange of bodily fluids.

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7
Q

Inoculation

A

-Where the skin is broken and microorganisms enter directly.

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8
Q

Ingestion

A

-Where infected food or drink is consumed.

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9
Q

Indirect transmission

A

-When a pathogen is passed through an intermediate stage.

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10
Q

Fomites

A

-Inanimate objects with pathogens on.

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11
Q

Droplet infection

A

-Transfer of pathogens through sneezing or coughing.

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12
Q

Vectors

A

-Move to transfer pathogens to other places.
-Eg mosquitoes, wind, water

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13
Q

Factors increasing rate of transmission

A

-Overcrowding.
-Poor nutrition.
-Compromised immune system.
-Poor waste disposal and sanitation.
-Warm, damp conditions.
-Poor, crowded infrastructure.
-Increased rainfall or wind speed.

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14
Q

Bodily barriers to stop infection

A

-Skin is a physical barrier, and changes pH outside of bacterial optimum.
-Blood clotting forms a fibrin scab to prevent bacteria from entering the wound.
-Mucous traps pathogens.
-Coughs and sneezes expel pathogens.
-Inflammation increases blood flow by making capillaries more permeable, allowing more phagocytes onto tissues.
-Saliva contains lysosomes to destroy pathogens.
-Ear wax traps pathogens
-Stomach acid denatures enzymes in pathogens.
-Fever raises the body temperature, making enzymes in pathogens less effective.

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15
Q

Neutrophil

A

-Most common phagocyte.
-Multi lobed nucleus.
-Do phagocytosis.

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16
Q

Macrophage

A

-Largest phagocyte.
-Large nucleus.
-Become macrophages in tissue.

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17
Q

Monocytes

A

-Less common phagocyte.
-In tissues such as in the alveoli.
-Does phagocytosis.

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18
Q

Process of phagocytosis

A

-Phagocyte is attracted by chemical signals called cytokines to a tissue with a pathogen.
-Attracted by chemicals called opsonins produced by the phagocyte.
-Phagocyte identifies pathogen as non-self.
-Phagocyte’s cytoplasm engulfs the pathogen.
-Pathogen is contained within a vesicle called a phagosome inside the cytoplasm.
-Lysosomes move into the phagosome and fuse with it, delivering digestive enzymes.
-Phagocyte displays the pathogen’s antigens, becoming an antigen-presenting cell.
-This activates the specific immune response.

19
Q

Secondary (specific) immune response

A

-Receptors on T-Lymphocytes bind to antigen of antigen-presenting-cell and are activated.
-Interleukins are produced by T-helper cells, which stimulate the production of more receptors complimentary to the antigen. This is known as clonal selection.
-T cells formed from clonal selection divide by mitosis.

20
Q

T-Killer cells

A

-Formed from division of T-cells formed in clonal selection.
-Destroy complimentary pathogens by using perforins to punch holes in their membranes.

21
Q

T-memory cells

A

-Formed from division of T-cells formed in clonal selection.
-Provides an immunological memory of specific pathogen.
-Can divide rapidly into many t-killer cells upon encountering the antigen a second time.

22
Q

T-regulator cells

A

-Formed from division of T-cells formed in clonal selection.
-Suppress the immune system after the pathogen is destroyed.
-Prevent autoimmune response from T-killer cells.

23
Q

T-helper cells

A

-Formed from division of T-cells formed in clonal selection.
-Can produce interleukins that either stimulate further phagocytosis or B-helper cells to divide.

24
Q

B-Lymphocyte activation/humoral immunity

A

-B-lymphocytes are activated through encountering its complementary antigen (clonal selection) or by T-helper cells.
-They divide by mitosis (clonal expansion)

25
B-effector cells
-Formed from division of B-cells in clonal expansion. -Divide by mitosis to form plasma cells.
26
B-memory cells
-Formed from division of B-cells in clonal expansion. -Provide an immunological memory. -Divide into many plasma cells upon second contact.
27
Plasma cells
-Formed from division of B-lymphocytes or B-effector cells. -Divide to produce thousands of antibodies per second. -Only live for a few days.
28
Antibody structure
-Smaller variable region that is complementary to one specific antigen. -Larger constant region that allows phagocytes to recognise and bind to the antibody. -A smaller light chain and longer heavy chain, bonded within and between with disulphide bonds. -A hinge region that provides flexibility, allowing two variable regions to bind to more than one pathogen.
29
Agglutination
-Antibodies cause pathogens to stick together. -Makes it easier for phagocytes to engulf pathogens.
30
Antitoxins
-Neutralise toxins produced by pathogens and prevent them from entering our cells.
31
Neutralisation
-Antibodies bind to viruses and stop their proteins from binding to host cells.
32
Opsonisation
-Antibodies bind to the surface of a pathogen and attract phagocytes.
33
Natural immunity
-Gained by having the disease or other natural means.
34
Artificial immunity
-Gained by man made means such as vaccination.
35
Passive immunity
-Provided without an immune response.
36
Active immunity
-Provided with an immune response.
37
Vaccination
-Either: -An injection of dead or inactive pathogens. -Or an injection of antigens from a pathogen. -Results in the production of B and T memory cells that prevent secondary infection. -Routine vaccinations include TB, measles, polio and meningitis.
38
Herd Immunity
-When a large number of people are vaccinated, meaning the pathogen is less likely to spread to unvaccinated people.
39
Ring vaccination
-Where populations in the area surrounding an outbreak are vaccinated to contain the spread of disease.
40
Autoimmune disease
-Where the body fails to recognise a tissue or organ as self, and attacks itself. -Eg lupus, type 1 diabetes. -Most have no cure, only immunosuppressant treatments.
41
Ways medicines are discovered
-Naturally occurring medicines in organisms such as fungus (penicillin) or willow trees (aspirin) -Synthetised medicines from genetically modified organisms (usually bacteria) that reproduce to create more medicines. -Pharmacogenetics, in which an individuals genetics are used to determine the most effective drugs.
42
Physical plant defences
-Thick cellulose cell wall. -Waxy cuticle prevents water from collecting on the surface. -Guard cells which prevent pathogens entering via stomata. -These are known as passive plant defences as they are present before infection.
43
Chemical defences of plants
-Terpenoids have antibacterial and antifungal properties. -Alkaloids are bitter compounds that prevent damage to the plant from herbivores. -Phenols and tannins deactivate digestive enzyme in insects (also antibiotic and antifungal) -Defensins inhibit action of ion transport channels. -Hydrolytic enzymes degrade bacterial cell walls. -Chitinase breaks down fungal cell walls.
44
Active plant defences.
-These are defences that occur after a pathogen is detected. -These include callose (phloem) and tylose (xylem) which are polysaccharides that are deposited into the vascular bundle to prevent flow across the plant. -Cell walls are thickened with additional cellulose. -Necrosis is deliberate cell death to limit the pathogen's access to water and nutrients.