Chapter 12 - Communicable Disease Flashcards

1
Q

What is a pathogen

A

Disease causing microorganism

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2
Q

Different types of pathogens

A

Bacteria
Fungi
Virus
Protoctista

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3
Q

Vector definition

A

Living or non living factor that transmits a pathogen from one organism to another

Water, mosquito

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4
Q

How do viruses infect

A

They take over cell metabolism
Viral DNA gets into the host
Their genetic material is inserted into host DNA
Uses host cell to make more viruses
Viruses reproduce rapidly and evolve to adapt to their host
Bust out of cell to infect others

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5
Q

What are protoctistas

A

Eukaryotic organisms

Need a vector to transfer them to their hosts

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6
Q

2 ways bacteria can be classified

A

By their shape

By their cell walls (gram staining)

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7
Q

What are fungi

A

Eukaryotic organisms
Multicellular
Saprophytes - feed on dead + decaying matter , can be parasitic

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8
Q

How do protoctistas infect

A

Take over cells and break them open

Digest the cells contents and use it to reproduce

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9
Q

How do fungi infect

A

Digest living cells and destroy them

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10
Q

How do bacteria infect

A

Produce toxins that damage the host cells by:

  • breaking cell membranes
  • damage enzymes
  • interfere with hosts cells genetic material - can’t divide
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11
Q

Diseases caused by bacterium

A

Bacterial meningitis
Tuberculosis
Ring rot

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12
Q

Diseases caused by protoctistas

A

Potato / tomato late blight

Malaria

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13
Q

Diseases cause by fungi

A

Athletes foot
Ringworm
Black sigatoka

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14
Q

Tuberculosis affects

A

Animals - human and cattle

Damages and destroys lung tissue
Suppresses the immune system

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15
Q

Diseases caused by viruses

A

Tobacco mosaic virus
HIV AIDS
influenza

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16
Q

Bacterial meningitis affects

A

Humans (kids)

Cause blood poisoning
Rash

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17
Q

Ring rot affect

A

Potatoes and tomatoes

Gram positive bacteria
Damages leaves, tuber and fruit

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18
Q

HIV affects

A

Humans

Targets t-helper cells in immune system
Destroys immune system

Transcripts RNA to single strand of DNA
interacts with genetic material

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19
Q

Influenza

A

Animals

Kills ciliated epithelial cells in gas exchange system
Airways open to infection

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20
Q

Tobacco mosaic virus

A

Plants

Damages leaves, flowers, fruit
Stunts growth

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21
Q

Black sigatoka

A

Banana plants

Attack’s and destroys leaves
Turn black

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22
Q

Ring worm

A

Cattle

Grey white crusty areas in skin
Itchy

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23
Q

Athletes foot

A

Humans

Grows on and digests warm moist skin
Causes cracking and scaling, itchy

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24
Q

Potato blight

A

Potatoes and tomatoes

Destroys leaves, tuber, fruits

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25
Malaria
Humans animals Female mosquitos Plasmodium passed on to people
26
What is direct transmission
Pathogen is transferred directly from one individual to another
27
Example of direct transmission
- Direct contact - Inoculation - through cuts, break in skin - Ingestion
28
What is indirect transmission
Pathogen travels from one individual to another via an intermediate
29
Examples of indirect transmission
Air , water, food, another object Fomites- inanimate objects (socks) Vectors- mosquitos Spores- in air and water Soil contamination
30
How do living conditions affect disease transmission
Overcrowded conditions increase disease transmissions TB - droplet infection (directly) - remain in air (indirectly)
31
How does climate affect disease transmission
Increased rainfall and wind - promote spread Damp warm conditions increase disease survival Potato late blight - spores spread Mosquitoes - warm - ideal for breeding
32
How social factors affect disease transmission
High when Limited access to: Healthcare Education
33
Preventing communicable disease in plants
``` Plant crops with space in between Clear fields throughly when harvesting Rotate crops Control insect vectors Hygiene practices - sterilising ```
34
How do plants recognise an attack
Receptors in cell membranes respond to molecules from pathogens Stimulates release of signalling molecules These trigger cellular responses by switching on genes Responses = producing defensive chemicals
35
What physical defences do plants have
-Waxy cuticle = barrier, stop water collecting on leaf - reduce infection transferred -Cell walls -produce Polysaccharide called CALLOSE = Deposited between cell wall and plasma membrane - harder for pathogens to enter - at plasmodesmata = limit spread of virus between cells - blocks sieve plates in phloem
36
What chemical defences to plants have
Produce antimicrobial chemicals (antibiotics) - kill invading pathogens, inhibit their growth - interfere with cell membranes - saponins / phytoalexins Secrete chemicals toxic to insects - reduces plant viruses carried by insect vectors - cyanide
37
How does skin prevent infection
blocks pathogens from entering body | produces antimicrobial chemicals - lower pH , inhibiting growth of pathogen
38
How does woUnd repair prevent infection
Skin can repair itself by reforming a barrier against pathogen entry - surface is repaired by outer layer of skin cells dividing and migrating to the edges of wound - tissue below contracts to bring edges closer together - repaired using collagen fibres
39
How does expulsive reflexes prevent infection
Sneezing and coughing - expel foreign objects from the body (mucous membrane) Vomiting and diarrhoea - expel contents of gut along with pathogens
40
How do fevers get rid of pathogens
Raise body temperature Inhibits pathogen reproduction Immune system works faster
41
How does Mucous membranes prevent infection
protect the body openings that are exposed to the environment secretes mucus that traps pathogens contains phagocytes contains lysozymes that destroy bacterial + fungal cell walls
42
How does blood clotting prevent infection
blood clot is a mesh of protein fibres take place when platelets are exposed to damaged blood vessels plug wounds prevent pathogen entry stop blood loss
43
How does inflammation prevent infection
damaged tissue activates mast cells that release histamines and cytokines ``` histamines increases the permeability of the blood vessels - leak fluid into surroundings - cause swelling * isolate the pathogens that have entered the damaged tissue cause vasodiliation - increases the blood flow - makes the area hot ``` cytokines - brings white blood cells to fight of pathogens
44
How is phagocytosis carried out Neutrophils and macrophages
Phagocytes are attracted to chemicals produced by pathogen Phagocytes recognise the pathogen as non self Phagocytes engulf pathogen by surrounding it with cell surface membrane until it pinches off to form vesicles called / cytoplasm moves around pathogen = phagosome Phagosome fuses with lysosome to form = phagolysosome Enzymes from lysosome digest and destroy pathogens
45
What are the 2 types of white blood cells
Neutrophils - multi lobed nucleus Macrophage
46
What is an antigen
Molecules found on the surface of cells that trigger immune response
47
How are antigen presenting cells formed Macrophages
Macrophage digests everything but antigens Combines the antigens from the pathogen surface membrane with glycoproteins in the cytoplasm called = Major Histocompatibility Complex = MHC The MHC complex moves these antigens to the macrophages surface membrane to become = APC
48
What is an APC
A cell that presents foreign antigens complexed with MHCs on its own cell surface membrane
49
What does MHC stand for
Major Histocompatibilty complexes
50
What do the cytokines released by phagocytes do
Proteins that act as messenger molecules Informing other phagocytes that the body is under attack Stimulating other phagocytes to move to infected area
51
Why are opsonins useful chemicals in phagocytosis
Chemicals that bind to pathogens and tag them So they’re more easily recognised by phagocytes Allow phagocytes to get closer to pathogens
52
Examining blood smears What will you see
Red blood cells Platelets = fragments of cells involved in blood clotting Neutrophils Monocytes Lymphocyte
53
Visible features of | Neutrophils
- Multi lobed nucleus | - Grainy cytoplasm
54
Visible features of Lymphocytes
- smaller than neutrophil | - nucleus takes up most space
55
Visible features of Monocytes
- Biggest white blood cell - Kidney bean shaped nucleus - No grainy cytoplasm
56
What is the structure of an antibody
Y shaped glycoprotein called immunoglobulin Made of 2 identical long polypeptide chains = heavy chain 2 dental short polypeptide chains = light chain Chains are held together by disulfide Hinge region = allows flexibility when the antigen binds to the antibody Binding site = variable site - gives specificity Allows binding to receptors on immune system = constant region
57
How do antibodies prevent the pathogen binding to human cells
- pathogens can’t invade host cells when part of an antigen-antibody complex by blocking the cell surface receptors the pathogen needs to bind to the host
58
Outline action or opsonins
- antigen-antibody complex acts as an opsonise so complex is more easily recognised an engulfed by phagocytes
59
Outline actions of agglutinins
- anti bodies act as agglutinins - causing pathogens carrying antigen-antibody complexes to clump together - prevents from spreading - easier for phagocytes to engulf at same time
60
Outline actions of antitoxins
Antibodies called antitoxins Bind to toxins produced by pathogens Prevent toxins from affecting human cells Toxins are neutralised
61
What is the function of antibodies
- acts as an opsonin - are agglutinins - can neutralise toxins - prevent from binding to human cells
62
What is active immunity
Immunity you get when your own immune system makes its own antibodies after being stimulated by antigens
63
What are the 2 different types of active immunity
Natural Artificial
64
What is a example of Natural active immunity
You become immune after catching a disease You produce your own antibodies
65
What is a example of Artificial active immunity
When you become immune after being given a vaccination A weakened or dead pathogen
66
What is passive immunity
Immunity you get from being given antibodies by a different organism
67
Example of Natural passive immunity
A baby gaining antibodies from mothers breast milk, or placenta Colostrum
68
Example of Artificial passive immunity
Immune after being injected with someone else’s antibodies If you have tetanus, you are injected with antibodies against the tetanus toxin, from blood donations
69
What are the differences between active and passive immunity
Active - long term - creates memory cells - takes time for protection to develop - requires exposure to antigen Passive - short term - takes immediate effect - doesn’t create memory cells - does not need antigens
70
What is cell mediated immunity
T lymphocytes respond to cells of an organism that have been altered
71
How does cell mediation work
Non specific defence of phagocytosis = produces APC The CD4 receptors on the T helper lymphocytes meets a complementary antigen on an APC and binds to it - This activated the T-helper cells in a process called CLONAL SELECTION Then undergoes CLONAL EXPANSION the T helper cells release interleukins and divide by mitosis and differentiate into different types of T cells that carry out different functions
72
What 4 things can cloned T cells do
Develop into T memory cells Develop into T killer cells They can release interleukins to increase phagocytosis They can release interleukins to stimulate the division of B lymphocytes Increases antibody production
73
Name the 4 different types of T lymphocytes
T killer T memory T helper T regulatory
74
What donT helper cells do
Their CD4 receptors bind to antigens on APC Release interleukins Which stimulate B cells Produce different T cells Stimulates macrophages to INGEST pathogens with antigen - antibody complex
75
What do T killer cells do
Destroy the pathogen carrying antigens By producing a chemical called = perforin That kills the pathogen By making holes in cell surface membrane Freely permeable
76
What do T memory cells do
Part of immunological memory Remembrer the specific antigens So when met again Will divide rapidly to produce specific T killer cells To destroy pathogen
77
What do T regulator cells do
Suppress the immune system From other white blood cells Once pathogen has been eliminated To prevent autoimmune response Interleukins important
78
What is humoral immunity
Produces antibodies to respond to foreign antigens
79
How does humoral immunity occur
B lymphocytes are covered with antibodies These antibodies join with the complementary antigens on the pathogen The B cell engulfs and processes the antigen to become a B cell APC T helper cells bind to the B APC = CLONAL SÉLECTION (B cell with correct antigen is selected for cloning) T cells produce interleukins that activate B Cells to divide by mitosis = CLONAL EXPANSION
80
Why do B cells differentiate into
Plasma cells B Effector cells B Memory cells
81
What do plasma cells do Primary immune response
Produce antibodies to a particular antigen Release them into circulation Disable antigens Act act opsonins, agglutinins, antitoxins
82
What do effector cells do
Divide to form plasma cell clones
83
What do B memory cells do Secondary immune response
Provide immunological memory Programmed to remember antigen Enables body to respond quickly when pathogen reenters
84
Why is the primary response slow
Antigens on pathogen active immune system Not enough B lymphocytes to produce right antibody Eventually will produce enough antibody - show symptoms After exposure to antigen T + B make memory cells
85
Why is the secondary response faster
Immune system produces stronger, faster response B Memory divide into plasma cells = make antibodies T Memory divide into T cells to destroy pathogen Before symptoms show
86
What is an auto immune disease
Response when the immune system acts against its won cells and destroys healthy tissue Recognises “self cells” as foreign
87
Rheumatoid arthritis
Joints Feet, wrists Cure = anti inflammatory , immunosuppressant, steroids
88
Lupus
Affects skin and joints Can attack organs Cure = immunosuppressant, anti inflammatory, steroids
89
What are the principles of vaccination
1) pathogen is made safe so no risk of infection - dead, inactivated, altered, attenuated 2) small amounts of safe antigen injected into blood 3) primary immune response triggered 4) memory cells made 5) come into contact again - secondary response is quicker and stronger
90
What is herd immunity
When most people in a community are vaccinated the disease become rare Even people without the vaccines are unlikely to get it Reduces the risk of an epidemic
91
What are routine vaccines
MMR = - measles , mumps , rubella - children Meningitis C vaccine = - protects against bacteria that causes Meningitis C - 3 months, 1 year, teenager
92
Reasons for changes in vaccines and vaccination programmes Influenza
Antigens on influenza surface change regularly Forming new strains of virus Memory cells from virus against 1 strain will not impact new strains New vaccines are made every year that are most effective against the recent circulating viruses
93
Why do possible sources of medicine need to be protected
Uses natural compounds Plants, animals, microorganisms Penicillin = fungus Cancer drugs = soil bacteria Alzheimer’s = daffodils
94
What are personalised medicines
Tailored to an individuals genes Doctor can predict how you will respond to medicine, and prescribe you the most effective using your genetic material
95
What is synthetic biology
Uses technology to design artificial proteins, cells, microorganisms Cancer - destroy cancer cells while leaving body healthy
96
Benefits of using antibiotics
Kill or inhibit growth of bacteria | Doesn’t damage human cells = isolated
97
Disadvantages of antibiotics
Can cause severe allergic reactions Can form antibiotic resistance - mutations occur so they become naturally resistant, spread the advantageous gene Prevent by not giving to small infections Making sure the course of medicine is ended so all bacteria is killed off
98
MRSA
Causes serious wound infection | Resistant to meticillin
99
Clostridium difficile
Harmless bacteria in digestive system killed, expect Cdifficile Produces cramps, fevers, diarrhoea