Communicable diseases Flashcards

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1
Q

What are non specific responses?

A

General and more immediate. Physical barriers and some cellular processes eg. phagocytosis.

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2
Q

What are specific responses?

A

Less rapid but longer lasting. Involve lymphocytes; T cells in cell mediated response and B cells in humoral response.

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3
Q

What is the role of skin as a primary defence?

A

Made up of cells = keratinocytes. Their cytoplasm is replaced by keratin protein in keratinisation on skin surface. Barrier to pathogens.
Harmless microbes = skin flora live on skin. Prevents pathogenic microbes from colonising by competing with them.

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4
Q

What is the role of blood clotting?

A

When the blood clot dries, it forms a temporary seal, allowing skin to repair.
Trigger blood clotting - platelets and damaged tissues release clotting factors which activate enzyme cascade. Fibrous collagen deposited under the scab and stem cells divide.

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5
Q

What are mucous membranes?

A

Exchange surfaces where oxygen and nutrients enter the blood are thinner + more exposed to pathogens. Protected by mucous membranes.
In airways, goblet cells and gland secrete mucous - traps pathogens. Ciliated epithelium.

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6
Q

What are other non specific defence mechanisms?

A

Explosive reflexes, non specific chemical defences, inflammation.

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7
Q

How do expulsive reflexes work?

A

Some pathogens can release toxins. When sensitive areas irritated - reflexes. eg. coughing, vomiting.

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8
Q

How do non-specific chemical defences?

A

eg. saliva and tears. Contain enzyme - lysozyme. Kills bacteria by breaking down bacterial cell wall. Lysis of pathogen stops it entering nose, eyes, mouth.

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9
Q

How does inflammation work?

A
  • pathogen detected in tissues by mast cells
  • triggers mast cells to release histamine –> vasodilation, capillary walls in tissues more permeable to WBCs
  • more WBCs can move out capillaries into tissue fluid and reach infection
  • more tissue fluid produced -> swelling
  • excess tissue fluid drained into lymphatic system where more immune cells stored
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10
Q

What is phagocytosis?

A

A specific type of WBC engulfs and digests pathogens to stop them causing damage. Used to remove dead, damaged and abnormal cells. eg. macrophages and neutrophils.

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11
Q

How do neutrophils work?

A

Have multi lobed nuclei.
- pathogen has chemical markers on cell surface membrane = antigens. Opsonins help phagocytes to carry out function.
- pathogen engulfed by phagocyte to form a vesicle = phagosome
- lysosomes within phagocyte fuse with phagosome, releasing lysozymes (hydrolyse cell walls)
- products absorbed by phagocytes

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12
Q

What are macrophages?

A

When neutrophils die, macrophages arrive at infected tissue and engulf pathogenic cells. Not fully digest pathogen. Movies antigen to special protein complex. Macrophage exhibits protein complex on cell surface and becomes antigen presenting cell.

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13
Q

How are phagocytes specialised?

A
  • phagocytes have well developed cytoskeletons - change shape to engulf pathogens and move lysosomes around
  • many mitochondria
  • many ribosomes to synthesise lysozymes
  • neutrophils have lobed nucleus to help them squeeze through narrows gaps
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14
Q

What is an antigen?

A

A membrane bound molecule used to recognise pathogens, which stimulates an immune response.

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15
Q

What is an antibody?

A

A specific protein produced by plasma cells that can attach to pathogenic antigens.

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16
Q

Why is there a variety of antibodies?

A

They have specific binding sites that bind to complementary antigen of a pathogen. Each type of antigen a complementary antibody exists.

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17
Q

What is the structure of antibodies?

A

Y shaped proteins made of 4 polypeptide chains. 2 long chains = heavy. 2 short chains = light. Disulphide bridges hold polypeptides together.
Variable region binds to antigen. Specific to antigen shape.
Constant region = same in all antibodies and can bind to receptors present on phagocytic immune cells.
Hinge region allows flexibility.

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18
Q

What are opsonins?

A

Proteins which attach to antigens on surface of pathogen. Non specific antibody and act as binding sites for phagocytes. Enhance their ability to bind and destroy pathogens.

Some made as part of specific immune response. Might be used by pathogen to attach to host cells - stop antigen functioning = neutralisation.

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19
Q

What is agglutination?

A

Agglutinins help immune cells destroy antigens more effectively.
1 antibody can bind to multiple antigens and cause pathogens to clump together = agglutination
Easier for multiple pathogens to be engulfed by a phagocyte + harder to enter host cells.

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20
Q

What is an anti-toxin?

A

Subset of antibodies can bind and neutralise toxins released by pathogens to prevent toxin causing damage.

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21
Q

What are the 2 categories of white blood cells?

A

Cells in non specific responses not distinguish between specific antigens. Respond against any infection for short term protection.
Lymphocytes with specific responses - adaptive response to destroy specific pathogen.

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22
Q

What is the structure and function of lymphocytes?

A

Large nucleus and specialised receptors on plasma membrane. Specific and LT protection. 2 types: T cells leave bone marrow and mature in thymus gland. B cells stay and mature in bone marrow.

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23
Q

What is clonal selection?

A

The selection of a specific B or T cell which is specific to the antigen.

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24
Q

What are the different types of T lymphocytes?

A

T helper cells release chemical messengers = cytokines - involved in stimulating phagocytosis + develop B lymphocytes.
T killer cells attack + kill host body cells displaying foreign antigen.
T memory cells stay in blood for years for LT immunity - fast response if infected again.
T regulator cells stop immune response after pathogen removed. Stop autoimmunity.

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25
Q

What are the 2 types of B lymphocytes?

A

Plasma cells circulate in the blood and secrete many antibodies.
B memory cells provide LT protection = immunological memory.

26
Q

What are cytokines?

A

Hormone-like molecules used in cell signalling to stimulate the immune response.

27
Q

What are the different types of cytokines?

A

Bind to cell surface receptors on target cells - complimentary depending on function.

Monokines released by
macrophages. Attract neutrophils and stimulate B cell differentiation.
Interleukins released by T cells and macrophages. Stimulate clonal expansion.
Interferon released by many cells. Inhibits viral replication and stimulate T killer cells.

28
Q

What is clonal expansion?

A

An increase in the number of T or B cells by mitotic cell divisions.

29
Q

What are the stages of the specific immune response?

A
  1. infection and reproduction of the pathogen
  2. antigen presentation - phagocytosis –> APC and on infected cells
  3. clonal selection - T + B lymphocytes detect antigen and carry corresponding receptor molecule
  4. clonal expansion
  5. differentiation - B + T cells develop
  6. action - T helper cells stimulate B cell division, T killer attack host cells, memory cells stay in blood, T regulator cells regulate response.
30
Q

What happens in the primary response?

A

Symptoms appear as initial response is slow. When infection gone, specific antibodies not stay in blood, but memory cells do.

31
Q

What happens in the secondary response?

A

B + T memory cells in blood recognise specific antigens from same pathogen. Antibodies made faster so conc of antibodies increases faster + is higher.
No symptoms.

32
Q

What is an autoimmune disease?

A

When immune system attacks own body. Any lymphocytes specific to self antigens are destroyed normally, but sometimes self-reactive lymphocytes escape + circulate. Highly damaging + even life treating.

33
Q

What are examples of autoimmune diseases?

A

Arthritis - antibodies attack membranes around joints. Painful inflammation + swelling.
Lupus - antibodies attack proteins in cell nucleus. Swelling and pain.

34
Q

What is vaccination?

A

The introduction into the body of a vaccine containing disease antigenic material, in order to stimulate an immune response to achieve immunity.

35
Q

How does vaccination work?

A
  1. vaccine delivered to body by injection/orally. Only small amount.
  2. immune system produces response against specific antigen + specific memory cells produced
  3. when active pathogen invades host for 1st time, memory cells differentiate into plasma cells
  4. rapid production of antibodies + infection rapidly overcome.
36
Q

What can vaccines contain?

A
  • Whole live pathogens - similar antigens to disease-causing pathogen.
  • Harmless/weakened version of pathogen.
  • Vaccine with only antigens from pathogen.
  • Dead pathogen - not cause disease.
  • Toxoid - harmless version of toxin produced by pathogen.
37
Q

What is herd immunity?

A

When vaccination of significant proportion of population provides protection for individuals who have not developed immunity.

38
Q

What is an epidemic?

A

The rapid spread of a disease through a high proportion of the population.

39
Q

What is an example of a monitored pathogen to prevent an epidemic?

A

Flu - mutates frequently so its antigens change. Vaccines have to be changed. New modified influenza vaccines are made each year, specific for mutated antigen.
Given to ‘at risk’ people.

40
Q

What is active immunity?

A

When specific antibodies produced by individuals own immune system. Direct contact with pathogen or its antigens is needed.
eg. vaccination

41
Q

What is passive immunity?

A

When specific antibodies introduced from outside source.
eg. mother to baby via breast milk

42
Q

What is natural immunity?

A

Via regular infection = natural active. They make antibodies.
Via breastfeeding = natural passive immunity.

43
Q

What is artificial immunity?

A

Induced by medical intervention without symptoms.
Vaccination provides artificial active immunity.
Injection of antibodies made by another organism = artificial passive.

44
Q

What is a virus?

A

Type of pathogen - acellular, non living. Smaller than bacteria and can only replicate inside living host cells. Hijack host cell protein production - make more copies of themselves.

45
Q

What are examples of viruses?

A

HIV - causes AIDS. Attacks immune cells, reducing efficacy of immune response.
Influenza - attacks mucous membranes in respiratory system. eg. muscle pains, coughing.
Tobacco mosaic virus - mottling and discolouration of leaves in infected plants eg. tobacco/tomato.

46
Q

What are fungal diseases?

A

Hyphae can release spores which allow fungi to reproduce.
eg. athletes foot, ringworm in cattle. Black Sigatoka in banana plants and causes leaf spots.

47
Q

What are protoctista diseases?

A

Blight in tomatoes + potatoes, affecting leaves and tubers.
Malaria caused by protoctist as parasite in blood –> headache + fever.

48
Q

What are bacterial diseases?

A

Tuberculosis - kills cells and tissues, commonly affecting lungs.
Bacterial meningitis - membranes around CNS –> swelling. Can damage brain + nerves.
Ring rot in tomatoes and potatoes. Vascular tissues decay and decreases crop yield.

49
Q

What are mechanisms of direct transmission?

A

Direct physical contact with infected person/contaminated surface. eg. athletes foot, HIV.
Ingestion of contaminated food/water. eg. cholera.
Droplet infection where pathogen carried in air in droplets between people. eg. TB, flu.
Fungal pathogens - spores carried in air or soil. eg. tetanus.

50
Q

How is malaria transmitted indirectly?

A
  • mosquito feeds on blood of infected human, takes in Plasmodium when parasite = gametocyte
  • in mosquito, gametocyte develops into infective stage. Migrate to salivary glands
  • mosquito feeds on healthy human + injects virus
  • travels to liver and reproduces
  • Plasmodium released into blood + infect RBCs - burst which stops O2 transport around body.
51
Q

What are factors affecting transmission?

A
  • warm, moist climate as best conditions for reproduction
  • overcrowding
  • poor health as less effective immune system
  • poor nutrition and homelessness
52
Q

What is antibiotic resistance?

A

Overuse over time -> spread of resistance. Over-prescription, use in farming + agriculture.
eg. MRSA = superbug as becoming rapidly resistant to new antibiotics made.
Most common in hospitals - threat to patients.

53
Q

How can antibiotic resistance be overcome?

A

Tightly control prescription of antibiotics - only given when needed.
Finish whole course of antibiotics so all bacteria destroyed.
Infection control measures in hospitals. eg. regular hand washing.

54
Q

Which medicines have come from plants?

A

Willow bark extract as painkiller. eg. aspirin and ibuprofen.
Morphine comes from unripe poppy seed heads. Reduce nervous action in CNS.

55
Q

How are new medicines from plants discovered?

A

Compounds produced by plants extracted + analysed to find main active ingredient. Concentrated + manufactured into drug. Maintain plant biodiversity as greater change of finding new drugs.

56
Q

What is personalised medicine?

A

Development of designer medicines for individuals. DNA sequencing for those with certain condition used to develop specific drug - best suited.
Or to discover new drugs from plants and microorganisms.

57
Q

What is synthetic biology?

A

Synthetic medicine is developing biological molecules and systems artificially.

58
Q

What are examples of passive plant defences?

A

Cellulose cell wall = physical barrier.
Cell walls thickened with lignin - waterproof and indigestible.
Waxy cuticle stops water collecting.
Bark on trees has lots of anti-pathogenic chemical defences eg. tannins.
Callose = large polysaccharide deposited in sieve plates. Prevents spread of pathogens if in phloem.
Guard cells close stomata.
Tylose in xylem can block it and stop pathogens spreading.

59
Q

What are examples of active plant defences?

A

More cellulose to cell walls.
Increase number of oxidative bursts - highly reactive O2 molecules - damage pathogens.
Close stomata to prevent further entry.
Induce cell necrosis around infection site, cutting off water and nutrient access.
Callose deposited preventing cellular penetration at infection site, strengthen cell wall and block plasmodesmata channels.

60
Q

What are different anti-pathogenic plant chemicals?

A

Terpenoids - oils with antibacterial + anti fungal properties.
Phenols - eg. tannins in tree bark stop insects by deactivating digestive and salivary enzymes.
Alkaloids -compounds which contain nitrogen (bitter to stop eating). Affect enzyme actions.
Defensins - cysteine rich, defensive proteins with anti microbial activity. Affect ion transport channel functioning.
Hydrolytic enzymes - in between cells. Chitinases break down chitin in cell walls, glucanases hydrolyse glycosidic bonds in gluocans, lysozymes destroy bacteria cell walls.