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Biology > Chapter 12 - Communicable Diseases > Flashcards

Chapter 12 - Communicable Diseases Flashcards

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1
Q

Communicable diseases

A

Disease can be passed on from one organism to another

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2
Q

Bacteria

A

➜ prokaryote
➜ rod shaped, spherical, comma shaped, spiralled, corkscrew
➜ produce toxins

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3
Q

Virus

A

➜ non living
➜ invades living body cells (the host)
➜ parasites
➜ takes over cell metabolism and causes cell to burst

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4
Q

Protist

A

➜ eukaryotic
➜ require a host - e.g mosquito
➜ digest and use cell contents as they reproduce

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5
Q

Fungi

A

➜ eukaryotic and multicellular
➜ prevent plants from photosynthesising
➜ reproduction causes many spores
➜ digest living cells
➜ e.g athletes foot and ringworm

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6
Q

Tuberculosis (mycobacterium tuberculosis) bacteria

A

➜ killing cells and tissue and phag in lungs
➜ lungs are most affected
➜ bacteria can be dormant due to it being inside a tubercles which is covered in thick waxy coat.
➜ when immune system is weakened bacteria will become active and destroy tissue slowly

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7
Q

Ring rot (sepedonicus) protist

A

➜ ring of decay in the vascular tissue of a potato tuber or tomato accompanied by leaf wilting

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8
Q

HIV/AIDS (human immunodeficiency virus) - virus

A

➜ attacks the immune system
➜ target T helper cells
➜ spread through bodily fluids

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9
Q

TMV virus

A

➜ causes mottling and discolouration of leaves

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10
Q

Malaria (Plasmodium falciparum) protist

A

➜ parasite in the blood that causes headache and fever and may progress to death
➜ caused by anopheles bite as the females are the ones that bite

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11
Q

Direct Contact

A

➜ kissing or any contact with bodily fluids
➜ skin to skin
➜ through faeces

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12
Q

Inoculation

A

➜ through a break in the skin
➜ animal bite
➜ sharing needles/puncture wounds

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13
Q

Ingestion

A

➜ contaminated food/drink
➜ uncooked food

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14
Q

Fomites

A

➜ inanimate objects
➜ bedding, socks etc etc

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15
Q

Droplet infection

A

➜ Coughing, sneezing, talking
➜ droplets may contain pathogen

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16
Q

Vectors

A

➜ transmits between hosts
➜ mosquitoes
➜ water

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17
Q

Factors affecting transmission of communicable diseases in animals

A

➜ poor nutrition
➜ overcrowding in living and working conditions
➜ compromised immune system (HIV/AIDS)
➜ poor disposal of waste (breeding site for vectors)
➜ climate change (tropical areas=more vectors)
➜ culture and infrastructure

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18
Q

Direct transmission (plants)

A

➜ Direct contact

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19
Q

Soil contamination (plants)

A

➜ infected plants can leave pathogens/reproductive spores in soil
➜ infect the next crop

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20
Q

Vectors (plants)

A

➜ wind - pathogen carried by wind
➜ water - pathogen carried by rivers/rain
➜ animals - as they feed it is carried
➜ humans - transmitted via clothes, hands, fomites, while transporting plants

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21
Q

Factors affecting the transmission of communicable diseases in plants

A

➜ planting variety of crop that are susceptible to disease
➜ overcrowding
➜ poor mineral nutrition
➜ damp warm conditions
➜ climate change - increased rainfall and wind = more transmission

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22
Q

Physical defences (plants)

A

➜ cellulose cell wall
➜ lignin thickening of cell walls
➜ waxy cuticles
➜ bark
➜ stomatal closure
➜ callose- blocks the flow in the sieve tube

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23
Q

Chemical defences

A

➜ insect repellent
➜ insecticides
➜ general toxins - chemicals made to be broken into cyanide compounds
➜ antifungal compounds
➜ antimicrobial compounds
➜ necrosis through intracellular enzymes

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24
Q

Non specific defences

A

➜ skin ➜ stomach acid
➜ mucous membranes ➜ mucus
➜ cilia
➜ Lysozymes
➜ eyelashes
➜ tears
➜ ear wax

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25
Q

Blood clotting

A

When there is a damaged blood vessel, platelets are activated by coming in contact with the collagen on the damaged blood vessel to secrete thromboplastin. This triggers a cascade of reactions leading to the common pathway, where thromboplastin, the enzyme, to associate with Ca^2+ as a cofactor to catalyse prothrombin to release thrombin. Thrombin is also an enzyme which catalyses fibrinogen into fibrin. Fibrin forms a network of fibres that trap the platelets and red blood cells to form a scab.

Extra: There is a release of clotting factors causing a secretion of prostaglandins such as serotonin, which constricts the damaged vessel.

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26
Q

Inflammatory response

A

➜ pain, heat, redness, swelling of tissue
➜ release histamines - increases permeability of blood vessels
➜ blood vessels leak fluid (antibodies, white blood cells and plasma leak out)
➜ this causes swelling and isolates any pathogens
➜ also causes vasodilation - increases blood flow - makes area hot and brings white blood cells to the area to fight off pathogens

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27
Q

Fevers

A

➜ when pathogen invades, hypothalamus makes temp go up
➜ specific immune system works better at higher temp
➜ pathogens reproduce below 37 degrees so prevents reproduction

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28
Q

Stages of Phagocytosis

A

➜ Pathogen produce chemical = attracts phagocytes
➜ Phago recognises protein on pathogen = response to non self organism
➜ Phago engulfs pathogen with the presence of opsonins and encloses it in a phagosome
➜ phagosome fuses with lysosome to form phagolysosome
➜ enzymes from lysosomes breaks down the pathogen
➜ phagocyte then presents pathogen’s antigens by attaching on surface to activate other immune system cells - acts as an antigen presenting cell APC (so other WBC know what to look out for)

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29
Q

T Lymphocytes - mature in thymus gland

A

➜ type of white blood cell
➜ T lymphs gain specific cell receptors called T cell receptors (TCRs)
➜ each T lymph has a different receptor on surface
➜ when receptor meets complimentary antigen, it binds to it, so each T lymph binds to diff antigen
➜ Macrophage and dendritic cells become APCs
➜ Once the correct T cell receptor is selected out of the different shapes it is activated. This is clonal selection.
➜ Selected T cell divides by mitosis to produce clones. This is clonal expansion.

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30
Q

Activated T lymphocytes

A

➜ T helper cells
➜ T killer cells
➜ T regulator cells
➜ T memory cells

31
Q

T helper cells

A

➜ produce interleukins (type of cytokine - cell signalling molecule) which stimulate the activity of B cells.
➜ This increases antibody production, production of other types of T cells and attracts & stimulates macrophages to ingest pathogens with antigen-antibody complexes.

32
Q

T killer cells

A

➜ destroy pathogen carrying antigen
➜ produce a chemical called perforin which makes hole in cell membrane to kill pathogen
➜ It then releases hydrogen peroxide

33
Q

T memory cells

A

➜ They live for a long time (immunological memory)
➜ If they meet an antigen for a second time they divide rapidly to form a huge number of clones of T killer cells to destroy pathogen

34
Q

T regulator cells

A

➜ supress the immune system, acting to control and regulate it
➜ stop immune response when pathogen is eliminated and makes sure body recognises self antigens and does not set up an autoimmune response

35
Q

B lymphocytes - mature in bone marrow

A

➜ type of white blood cell
➜ B lymphs gain specific cell surface receptors (BCRs)
➜ receptors = similar structure to antibodies
➜ each B lymph has a diff shaped antibody on the surface and will bind to diff antigens - antibody molecules do not leave B lymph but remain in cells surface membrane
➜ Macrophage and dendritic cells become APCs
➜ B cells also respond to smaller soluble antigens floating freely in blood
➜ Once the correct B cells with B cell receptor is selected out of the different shapes it is activated. This is clonal selection.
➜ Selected B cells divide by mitosis to produce clones - Clonal expansion

36
Q

Activated B cells

A

➜ Plasma Cells
➜ B effector cells
➜ B memory cells

37
Q

Plasma Cells

A

➜ secrete loads of antibody = specific to antigen into blood
➜ bind to antigen and form lots of antigen-antibody complexes
➜ T helper cells release interleukin which stimulates B cells to produce plasma cells

38
Q

B effector cells

A

➜ divide to form the plasma cell clones

39
Q

B memory cells

A

➜ live for long time (immunological memory)
➜ programmed to remember specific antigen and enable body to make a rapid response if pathogen encountered again

40
Q

Opsonisation

A

➜ antibodies attach to bacteria making them readily identifiable to phags
➜ once identified the phag has receptor proteins for the heavy polypep chains of the antibodies which enables phagocy to occur
➜ antibodies can attach to flagella to make them less active

41
Q

Agglutinating pathogens

A

➜ each antibody has 2 binding sites
➜ can bind to 2 pathogens at the same time, pathogens become clumped together
➜ phago then bind to the antibodies and phagocytose many pathogens at once
➜ antibodies can create holes in cell walls of pathogens and cause them to burst (lysis) when water is absorbed by osmosis

42
Q

Neutralising toxins

A

➜ toxins have different shapes
➜ antibodies bind to toxins produced by pathogens
➜ prevents toxins from affecting human cells so they are neutralised
➜ toxin-antibody complexes are also phagocytosed

43
Q

Preventing the pathogen binding to human cells

A

➜ when antibodies bind to antigens on pathogens, they may block cell surface receptors that the pathogen needs to bind to host cells
➜ pathogen can’t attach or infect host cells

44
Q

Primary response

A

➜ antigen on surface of pathogen activate immune system
➜ slow - not many B lymphs to make antibody needed
➜ while body produces enough antibodies - person experiences symptoms
➜ T and B lymphs produce memory cells - remain in body long time
➜ Memory T lymphs recognise specific antigen second time
➜ Memory B lymphs record specific antibodies needed for pathogen
➜ person = immune = can respond quickly to infection

45
Q

Secondary response

A

➜ fast - immune system remembers first infection
➜ clonal selection occurs faster - memory B lymphs activate and divide into plasma cells that produce the right antibody
➜ memory T lymphs activate and divide into correct T lymph to kill cell with antigen
➜ gets rid of pathogen before symptoms appear

46
Q

Antibodies

A

➜ globular glycoproteins called immunoglobulins
➜ quaternary structure - Y shaped, two Long polypeptide chains bonded by disulfide bonds to two short polypeptide chains
➜ each polypep chain has a constant region (do not vary and determines mechanism used to destroy the antigens) and variable region
➜ 5 classes of mammalian antibodies
➜ amino acid sequence in variable region (tip of Y) are different for each antibody. Variable region = where antibody attaches to antigen
➜ end of variable region = antigen binding site (110 to 130 amino aids)
➜ sites are specific to the epitope (part of the antigen that binds to antibody)
➜ hinge region (where disulfide bonds join chains) gives flexibility to antibody molecule allowing antigen-binding site to be placed at different angles when binding to antigens (NOT ALWAYS PRESENT IN ALL CLASSES OF ANTIBODIES)

47
Q

Active immunity

A

➜ acquired when an antigen enters body triggering specific immune response
➜ naturally acquired through exposure to microbes or artificially acquired via vaccines
➜ During primary response to a pathogen (natural) or to a vaccination (passive), antibody conc in blood takes 1 or 2 weeks to increase
➜ If body is invaded by same pathogen again or pathogen person was vaccinated against, during secondary response antibody conc in blood takes a much shorter period of time to increase and is higher than after the vaccination or first infection

48
Q

Passive immunity

A

➜ acquired without immune response - antibodies are not produced
➜ no immune system activation = no memory cells to produce secondary response
➜ Depending on disease, person may not have time to acquire immunity
➜ Passive also occurs artificially or naturally
➜ Artificial passive immunity occurs when people are given an injection/transfusion of antibiotics (e.g tetanus - antitoxins injected)
➜ Natural passive immunity occurs when fetus receives antibodies across placenta from mum OR babies receive initial breast milk from colostrum (IgA)

49
Q

Lupus - autoimmune disease

A

➜ butterfly rash across face
➜ women tend to suffer from disease more than men
➜ connective tissue of body is attacked by immune system - areas affected include joints, kidneys, heart, lungs and skin
➜ long term destruction

50
Q

Rheumatoid arthritis - autoimmune disease

A

➜ solely affects joints
➜ begins in fingers and hands and spreads to shoulders
➜ symptoms include muscle spasms, inflamed tendons, lethargy and constant joint pain

51
Q

Cause of autoimmune disease

A

➜ not very well known
➜ environmental factors (e.g moving from low autoimmune disease prevalence to areas of higher autoimmune disease prevalence) show an increased chance of developing autoimmune disease
➜ genetic factor (Susceptibility to an autoimmune disease was shown to be inherited)

52
Q

Vaccine

A

➜ a suspension of antigens that are intentionally put into the body to induce artificial active immunity
➜ 2 types:
- Live attenuated
- Inactivated
➜ can be administered via injection or orally
➜ vaccinations given by injection can be into a vein or muscle
➜ produce long-term immunity as they cause memory cells to be created therefore there is a faster, stronger secondary response
➜ international travel risks the possibility that a disease is reintroduced in a country
➜ some people can have poor response to it

53
Q

Antigenic Variation

A

➜ the variation (due to major changes) in the antigens of pathogens causes the vaccine to not trigger an immune response or diseases caused by eukaryotes (e.g malaria) have too many antigens on their cell surface membrane making it difficult to produce vaccines that would prompt immune system quickly enough

54
Q

Antigenic drift

A

➜ over time there are small changes in the structure and shape of antigens (within the same strain of virus)

55
Q

Antigenic shift

A

➜ there are major changes in antigens (within the same strain of virus)

56
Q

Antigenic concealment

A

➜ The pathogen ‘hides’ from the immune system by:
- Living inside cells
- Coating their bodies in host proteins
- Parasitising immune cells such as macrophages and T cells (eg. HIV)
- Remaining in parts of the body that are difficult for vaccines to reach (eg. Vibrio cholerae – cholera, remains in the small intestine)

57
Q

Cross breeding

A

➜ different strains of the virus invade the same cell, producing new viruses with antigens from different strains (essentially the strains swap antigens with each other)

58
Q

Herd immunity

A

➜ when a sufficiently large proportion of the population has been vaccinated
➜ Those who are not immunised are protected and unlikely to contract it as the levels of the disease are so low
➜ herd immunity can break down if vaccination rates fall

59
Q

Ring immunity

A

➜ People living or working near a vulnerable (or infected) person are vaccinated in order to prevent them from catching and transmitting the disease
➜ vaccinated individuals do not spread the pathogen onto others so individuals “within the ring” are protected as the people they interact with will not have the disease

60
Q

Challenges of eradication of disease

A

➜ sometimes pathogens are simple too complicated to form a vaccine for
➜ unstable political situations - due to war etc
➜ lack of public health facilities - poor infrastructure or few trained personnel etc

61
Q

Live attenuated vaccines

A

➜ contain pathogens that have been weakened
➜ weakened pathogen multiply slowly allowing body to recognise antigen and trigger primary response
➜ tend to produce a stronger and longer lasting immune response
➜ unsuitable for those with weak immune systems - pathogen may replicate too fast and enough antibodies aren’t produced

62
Q

Inactivated vaccines

A

➜ whole pathogens that have been killed or small parts of pathogen
➜ no living pathogen = no disease caused
➜ do not trigger a strong or long lasting immune system
➜ repeated doses or boosters are required
➜ Some people may have allergic reactions or local reactions (eg. sore arm) to inactivated vaccines as adjuvants may be conjugated to the subunit of the pathogen to strengthen and lengthen the immune response

63
Q

Discovering new drugs

A

➜ due to antibiotic resistant bacteria
➜ how:
- analysis of organism genome
- identifying molecules that fit into drug targets receptors and hormones or neurotransmitters and synapses
- modifying drugs that alr exist

64
Q

Microorganisms and plants as source of medicine

A

➜ bacteria and fungi have provided many antibiotics
➜ Plants = major source of drugs ( e.g Artemisinin, Quinidine etc)
➜ continued use of plants for drugs is an argument for maintaining biodiversity

65
Q

Personalised medicine

A

➜ involves the development of more targeted and personalised drugs to treat a variety of human diseases
➜ Human genome project (HGP) used to develop genomic medicine
➜ Genomic medicine uses information about an individuals genes to influence their clinical care
➜ information gained from genetic testing could be used to divide the population into subgroups according to how they are likely to respond to specific drugs. This would ensure that individuals receive the most effective drugs that cause the least side effects
➜ genetic screening - allows individuals with a high chance of developing a disease to be identified and preventative measures to be put in place

66
Q

Synthetic biology

A

➜ recent area of research that aims to create new biological parts, devices, and systems, or to redesign systems that already exist in nature
➜ more complex than genetic engineering

67
Q

Producing artemisinin

A
  • The most well-known use of synthetic biology is the commercial production of artemisinin
  • an antimalarial drug that is difficult to produce in other ways
  • E.coli and yeast are completely genetically reprogrammed so that they produce the precursor of the drug on a large scale
68
Q

Antibiotics

A

➜ chemical substances that inhibit or kill bacterial cells with little or no harm to human tissue
➜ antibiotics are derived from naturally occurring substances that are harmful to prokaryotic cells but not eukaryotic cells
➜ penicillin is the first antibiotic discovered in 1928 - Alexander Fleming
➜ either described as being bactericidal (they kill) or bacteriostatic (they inhibit growth processes)
➜ some antibiotics are derived from fungi while others are synthetic or semi-synthetic
➜ Broad-spectrum antibiotics act on a wide range of bacteria while narrow-spectrum antibiotics act on a very small number of bacteria

69
Q

Consequences of antibiotic resistance

A

➜ antibiotics are becoming less effective for many reasons, the main being:
- Overuse of antibiotics and antibiotics being prescribed when not necessary
- Large scale use of antibiotics in farming to prevent disease when livestock are kept in close quarters, even when animals are not sick
- patients failing to complete the full course of antibiotics prescribed by doctors
➜ Bacteria living where there is widespread use of many different antibiotics may have plasmids containing resistance genes for several different antibiotics, giving them multiple resistance
➜ resistance may first appear in a non-pathogenic bacterium, but then be passed on to a pathogenic species by horizontal transmission

70
Q

Staphylococcus aureus

A

➜ most common example of a resistant bacteria is a strain of Staphylococcus aureus that has developed resistance to a powerful antibiotic, methicillin and is now known as MRSA
➜ some strains have also become resistant to other antibiotics
➜ S.aureus usually lives on human skin, without causing disease however when there is an opportunity for the pathogen to enter the body they can cause serious disease

71
Q

Clostridium difficile

A

➜ bacteria present in the human gut
➜ numbers of C.diff are usually kept low due to the presence of other gut bacteria
➜ course of antibiotics can kill these ‘friendly’ gut bacteria, allowing C.diff to increase in numbers
➜ infection can cause diarrhoea and fever as they disrupt the epithelium of the intestine

72
Q

Reducing antibiotic resistance & its impact

A

➜ tighter control in countries where antibiotics are sold with no prescription
➜ doctors avoiding overuse of antibiotics - prescribe only when needed
➜ antibiotics not being used in non serious infections
➜ patients MUST finish entire course (so no left over bacteria don’t mutate to become resistant)
➜ antibiotics not being used for viral infections
➜ reduce the use of wide spectrum antibiotics and use antibiotic that are highly specific to infection
➜ change antibiotic prescribed each time

73
Q

The spread of already-resistant strains can be limited by:

A

➜ good HYGIENE - hand washing, hand sanitizers
➜ isolating infected patients
(think about covid and all the measures we took)

Biology (25 decks)

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