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Biology > Communicable diseases > Flashcards

Communicable diseases Flashcards

1
Q

toxins

A

chemicals that damage host cells and tissues leading to symptoms of a disease

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2
Q

bacteria as pathogens

A
  • most common organism for infection
  • not all bacteria are pathogens
  • prokarytotes - no membrane bound organelles
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3
Q

viruses as pathogens

A
  • non-living
  • no cellular structure
  • consist of DNA or RNA wrapped in a protein called a capsid
  • have attachment proteins to allow them to attach to host cells
  • can’t reproduce outside host cell
  • to reproduce, it attaches to host cell, passes through cell membrane, copies itself using enzymes of host cell
  • virus particles leave host cell and infect new host cells
  • prevent host cell functioning normally
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4
Q

fungi as pathogens

A
  • obtain nutrients by releasing enzymes and digesting dead material around them - fungi called saprophytes
  • products of digestion absorbed back into fungal cells
  • digestion causes damage to host cells and tissues
  • when they reproduce they release lots of spores so reproduce rapidly
  • in plants they infect leaves preventing photosynthesis
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5
Q

protists

A
  • eukaryotic cells
  • often require a vector to transfer disease
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6
Q

skin - non-specific defences for animals

A
  • protective layers - difficult for pathogens to penetrate
  • covered in oily sebum - prevents growth of harmful bacteria
  • covered in harmless microorganisms - reduce growth of pathogens by competing for resources
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7
Q

openings to body - non-specific defences for animals

A
  • lined with mucous membrane - traps microorganisms
  • mucous contains lysozyme - destroys bacteria by digesting cell wall
  • tears contain lysozyme
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8
Q

stomach - non-specific defences for animals

A
  • contains hydrochloric acid - kills pathogens in food or water
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9
Q

expulsive reflexes - non-specific defences for animals

A
  • sneezing, coughing, vomiting, diarrhoea
  • body tries to expel pathogen
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10
Q

blood clotting - non-specific defences for animals

A
  • involves platelets - tiny, short lived fragments of cells, no nucleus
  • if endothelium surrounding blood vessel is damaged, platelets exposed to proteins outside endothelium - activates them
  • platelets form plug around damaged area and release clotting factors eg. thromboplastin
  • thromboplastin and calcium ions act on prothrombin converting it into thrombin
  • thrombin acts as soluble blood protein called fibrinogen catalyses formation of fibrin (insoluble)
  • fibrin forms a mesh trapping RBC and forming a clot
  • platelets also release serotonin - causes smooth muscle cells in cell wall to contract - narrows it, reduces blood flow to area
  • scab formed keeping pathogens from entering while skin cells divide underneath
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11
Q

inflamation - non-specific defences for animals

A
  • tissue is damaged - activates mast cells - release histamines and cytokines
  • histamine causes blood vessels vasodilation - increased blood flow to area - red and hot - reduces pathogen ability to reproduce, makes blood vessel walls more permeable - more blood plasma leaves making more tissue fluid - swells, is painful
  • swelling is called an oedema
  • cytokines - attract WBC to carry out phagocytosis of pathogens
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12
Q

fever - non-specific defences for animals

A
  • increase in body temperature caused by cytokines going to hypothalamus
  • reduces ability of pathogens to reproduce
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13
Q

stages of phagocytosis - neutrophil

A
  • blood has opsonins (eg. antibodies) that recognise foreign antigen on pathogen
  • they stick to the pathogen, tagging it as foreign
  • phagocytes attracted to pathogens and receptor attaches to it
  • phagocyte engulfs pathogen - cytokines released, signalling to phagocytes to move to site of infection
  • pathogens now in phagosome
  • lysosomes move towards phagosome and fuse with it forming phagolysosome
  • lysozymes break down pathogen and destroy it
  • broken down pathogen moves out cell by exocytosis
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14
Q

phagocytosis - macrophage

A
  • pathogen engulfed into phagosome - cytokines released, signalling to phagocytes to move to site of infection
  • lysosomes fuse forming phagolysosome
  • lysozymes digest pathogen
  • glycoproteins (MHC) in cytoplasm move to phagolysosome and bind to antigen - MHC-antigen complex
  • MHC-antigen complex moves to cell membrane and antigens presented to exterior of cell
  • macrophage is antigen-presenting cell (APC)
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15
Q

what are phagocytes, types?

A
  • macrophages, neutrophils
  • part of non-specific defences
    (macrophages also in specific defences)
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16
Q

what immune system are lymphocytes part of?

A

specific immune system
B and T lymphocytes

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17
Q

antigen

A
  • proteins and polysaccharides on surface of pathogen cells - detected by immune cells as foreign
  • leads to an immune response - antibodies released
  • your own body cell’s antigens are recognised as ‘self’ and don’t produce and immune response
18
Q

antibody structure

A
  • glycoproteins with 4 polypeptide chains
  • 2 long heavy chains on inside - identical
  • 2 shorter light chains - identical
  • identical chains held to each other by disulfide bridges
  • 2 antigen binding sites (top of Y shape)
  • every antibody can bind to 2 identical antigens - antigen-antibody complex
  • antibodies specific to antigen they bind to
  • hinge region is flexible - allows distance between binding sites to vary
  • all antibodies have the same constant region and different variable regions
  • variable regions different for antibodies produced by different B lymphocytes
19
Q

function of antibodies

A
  • produced by B lymphocytes
  • humoral immunity
  • act as opsonins - tagging foreign bodies for phagocytes
  • stick pathogens together preventing them from spreading around body - agglutination
  • stick to pathogens such as viruses preventing them invading host cells
  • stick to bacterial toxins preventing them harming body cells (these antibodies called antitoxins)
20
Q

where are T lymphocytes produced and released?

A
  • produced in bone marrow
  • mature in thymus gland in chest
  • released into blood stream
21
Q

role of T lymphocytes in cell-mediated response

A
  • recognise antigen presenting cells - if it has correct T cell receptor for that antigen:
  • cell infected with virus, antigen from virus attached to MHC and presented on infected cell
  • cancer cell produces abnormal protein, attaches to MHC, presented on cell surface
  • transplanted cells have non-self antigen attached to MHC
  • when macrophage engulfs pathogen, antigen presented on surface
22
Q

T helper cell function in cell-mediated response

A
  • T cell receptor attaches to antigen on APC
  • T helper cell is activated and undergoes mitosis - identical clones produced
  • activated T helper cells produce cytokines then interleukins - trigger more phagocytes to increase rate of phagocytosis
  • activated T helper cells produce cytotoxic T cells - attach to infected cell and release perforin - forms holes in cell membrane causing destruction
  • T memory cells - rapidly divide into cytotoxic T cells if infected with same pathogen again
23
Q

T regulator cells

A
  • down-regulate immune system once pathogen destroyed
  • ensure body doesn’t attack self-antigens
  • reduced chances of autoimmune disorders
24
Q

Humoral response

A
  • 1 of 10 million B cells will have complementary antibody for specific antigen
  • B cell takes in antigen by endocytosis and presents it on membrane
  • B cell collides with specific T helper cell - activates B cell to undergo clonal selection
  • B cells undergo mitosis making clones that differentiate into plasma cells or memory cells
  • plasma cells - produce antibodies (short-lived)
  • memory cells - can divide rapidly into plasma cells if re-infection of same pathogen occurs (live for decades)
25
Q

natural active immunity

A
  • normal immune response with B and T lymphocytes
  • natural - body brings it about itself
  • active - body brings response producing antibodies etc.
26
Q

artificial active immunity

A
  • vaccinations - contain dead or weakened pathogen stimulating release of antibodies and memory cells
27
Q

natural passive

A
  • new born babies don’t have developed immune system
  • as a fetus, baby receives antibodies from mother through placenta
  • breast milk rich in antibodies
  • temporary
28
Q

artificial passive immunity

A
  • injected with antibodies produced by another organism
  • eg. tetanus - given antibodies from horses
  • temporary
29
Q

vaccinations

A
  • contain antigens from pathogen
  • some are weakened strain from bacteria or virus - infects patient but easily fought off by immune system
  • some are killed bacterial cells or inactivated virus - doesn’t cause infection but does cause immune response
  • some contain only antigen molecules
  • some contain modified toxin molecules
30
Q

graph showing antibody production and vaccination over time

A
  • vaccine enters body - primary immune response produces antibodies and T and B memory cells
  • in second immune response, antibodies produced rapidly and pathogen destroyed before symptoms
31
Q

importance of herd immunity

A
  • vaccinated people can’t catch disease and pass pathogen onto unvaccinated people
  • if enough population vaccinated, provides protection for unvaccinated people
32
Q

autoimmunity

A
  • when lymphocytes start attacking self-antigens
  • eg. type 1 diabetes - destroys beta cells in pancreas - can’t control conc. of glucose in blood
  • steroids, anti-inflammatory drugs etc. can reduce symptoms
33
Q

how does penicillin work?

A
  • interferes with petidoglycan in cell wall of bacterial cells
  • causes cells to burst
34
Q

why do antibiotics not effect human cells?

A
  • very different to bacterial cells eg. no cell wall, different ribosomes
35
Q

why do antibiotics have no effect on viruses?

A
  • viruses don’t contain any target molecules for them to act upon
  • they use a host cell to manufacture proteins and reproduce
36
Q

antibiotic resistance

A
  • caused by overuse of antibiotics
  • bacterium develops mutation for antibiotic resistance
  • in presence of antibiotic, all other bacteria are killed apart from resistant one
  • over time, resistant bacterium reproduces and there is large no. of resistant bacteria
  • eg. MRSA - staphylococcus bacteria resistant to methicillin
37
Q

HIV structure

A
  • RNA virus with 2 RNA strands found in protein capsid with enzymes
  • has lipid envelope with attachment proteins - allow it to attach to host cell
  • matrix proteins - help maintain structure of virus
38
Q

how does HIV cause symptoms?

A
  • once infected, HIV circulates blood - HIV positive
  • attachment protein attaches to molecule on surface of T helper cells
  • HIV lipid envelope fuses with cell membrane - capsid passes into cell
  • reverse transcriptase enzyme converts RNA to DNA which moves into cell nucleus and integrates with host DNA
  • HIV DNA becomes active and produces mRNA and HIV RNA genome
  • RNA moves to cytoplasm and is translated into proteins
  • virus particles assemble and bud from T helper cell, leave T helper cell with a cell membrane
  • leads to death of T helper cells - immune system an’t function - AIDS
39
Q

HIV treatment

A
  • can’t use antibiotics
  • antiviral drugs - inhibit reverse transcriptase
40
Q

sources of antibiotics

A
  • penicillin found in a fungus
  • aspirin discovered in willow trees
  • digoxin discovered in foxgloves
  • reduction of biodiversity threatens production of antibiotics
41
Q

synthetic biology

A

bacteria and other organisms can be genetically engineered to synthesise large quantities of drugs

42
Q

method of cloning

A

micropropagation

Biology (11 decks)

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