M4, C12 Communicable Diseases Flashcards
Define
a) communicable disease
b) pathogen
c) vectors
Communicable disease – can be passed from one organism to another
Pathogen – disease causing micro-organism
Vectors – carry pathogens from one organism to another (water/insects)
How do viruses cause disease?
1) VIrus attaches to host cell
2) It inserts genetic material / viral nucleic acid
3) The viral nucleic acid replicates
4) synthesis of viral protein
5) Virus particles assemble
6) they leave the host cell
They use the cell’s metabolism to replicate
how is bacteria classified?
Shape – rod, spherical, comma, spiralled, corkscrew
Cell walls – have different structures and react with gram staining differently, which affects how they react to antibiotics
Gram positive bacteria – purple under light microscope (MRSA)
Gram negative bacteria – red under light microscope (E.coli)
what increases the risk of catching a disease in plants
- Planting varieties of crops susceptible to disease
- Overcrowding
- Poor mineral nutrition reduces resistance
- Damp, warm conditions increase survival of pathogens
- Climate change – increased rainfall + wind, promote the spread
what are the two lines of defence in mammals
The primary non-specific defence (always present/activated rapidly)
The specific immune response (specific to each pathogen)
how does skin keep pathogens out
prevents entry, has skin flora (healthy microorganisms that outcompete pathogens, produces sebum (inhibits growth)
how does mucus membrane keep pathogens out
secrete sticky mucus, traps pathogens (contains phagocytes), contains lysozyme (destroys cell walls)
how does tears and urine keep pathogens out
contains lysosomes
how does stomach acid keep pathogens out
kills pathogens
what expulsive reflexes does our body do
Coughs and sneezes from gas exchange system
Diarrhoea and vomiting expel contents of gut
what is the process of blood clotting
When you cut yourself:
-Platelets come in contact with collagen in the skin
-Platelets stick to each other
-Secrete several substance
Thromboplastin – enzyme that initiates a cascade of reactions to the formation of a blood clot
Serotonin – causes smooth muscle in walls to contract (narrowing reduces blood supply to area
-Clot dries out, forming a hard, tough scab
-Epidermal cells below start to grow, sealing wound permanently
-Damages blood vessels regrow
-Collagen fibres deposited to give new tissue strength
what is
- thromboplastin
- prothrombin
- thrombin
- fibrinogen
- fibrin
Thromboplastin - enzyme
Prothrombin - clotting factors made by the liver
Thrombin - enzyme that converts fibrinogen to fibrin
Fibrinogen - is a glycoprotein
Fibrin - is a fibrous, non-globular protein
what is the body’s inflammatory response
= Pain, heat, redness and swelling of tissue
Mast cells (type of WBC) in damaged tissue release
–Histamine
Causes blood vessels to dilate and walls to become leaky (leak out tissue fluid) this tissue fluid causes swelling. Also raised temp (localised heat and redness) helps prevent pathogens reproducing.
–Cytokines
Attract phagocytes to the site
How does histamine cause the symptoms of inflammation?
Blood vessels dilating, causes localised redness and heat, so raises temperature to prevent pathogen reproducing
Blood vessels leaky to force blood plasma out, tissue fluid causes swelling and pain
what is the process of phagocytosis
1) phagocyte is attracted by chemicals produced by the pathogen
2) phagocyte recognises pathogen as non-self and binds to it
3) phagocyte engulfs the pathogen to form phagosome - lysosome moves towards phagosome and combines with it forming a phagolysosome
4) In phagolysosome, enzymes break down the pathogen
5) Digested pathogen absorbed by phagocyte - antigens combine with MHC in the cytoplasm
6) MHC is displayed on phagocyte membrane, making an antigen presenting cell (APC)
what is cytokines
A chemical produced by phagocytes that have engulfed a pathogen
They act as cell-signalling molecules, informing other phagocytes that the body is under attack and it stimulates them to move to the site of infection/inflammation
They can also increase body temp
what is opsonins
chemicals that bind to pathogens and ‘tag’ them so they can be more easily recognised by phagocytes.
phagocytes have receptors on their cell membranes that bind to common opsonins and the phagocyte then engulfs the pathogen.
what are antibodies made up of
two identical long polypeptide chains called the heavy chains and to much shorter identical chains called light chains.
they are held together by disulphide bridges and there are also disulphide bridges between the polypeptide chains to hold them in shape
how do antibodies bind to antigens
lock and key mechanism
the variable region of the antibody is the binding site and this gives the antibody a different shape to other antibodies because each antibody is specific to an antigen
the rest of the antibody is called the constant region as its always the same
when an antibody binds to an antigen it forms an antigen-antibody complex
what are the 4 ways in which antibodies defend the body
1) the antibody acts as an opsonin so the pathogen is easily engulfed and digested by phagocytes
2) stop them entering host cells
3) antibodies act as agglutinins which cause pathogens to clump together which stops them spreading and so phagocytes can engulf them at the same time
4) they act as antitoxins which bind to toxins produced by the pathogens and make them harmless
what are the two types of lymphocytes and where are they made
B lymphocytes - mature in the bone marrow
T lymphocytes - mature in the thymus gland
what are the main types of T lymphocytes
T helper cells
T killer cells
T memory cells
T regulator cells
what are the main types of B lymphocytes
plasma cells
B effector cells
B memory cells
what are T helper cells
they have receptors on their cell-surface membrane which bind the surface antigens on APCs
they produce interleukins which are a type of cytokine - they stimulate activity of B cells which increases antibody production ad stmulates other types of T cells
attracts and stimulates macrophages to ingest pathogens
what are T killer cells
destroy the pathogen carrying the antigen
produce a chemical called perforin which makes holes the cell surface membrane of the pathogen so it is freely permeable
what are T memory cells
part of the immunological memory
if they meet a pathogen for a second time they divide rapidly to form a huge number of clones to kill the pathogen
what are T regulator cells
they suppress the immune system - control and regulate it
stop the immune response once a pathogen has been eliminated
makes sure the body recognises self antigens and doesn’t set up an autoimmune response
what are plasma cells
produce antibodies to a particular antigen and release them into circulation
produces 2000 antibodies per second
what are B effector cells
divide to from plasma cell clones
what are B memory cells
provide immunological memory
programmed to remember a specific antigen and enable the body to make a rapid response when that antigen on a pathogen is encountered again
in cell-mediated immunity how could cells have been changed
viral infection
mutation
antigen processing
what happens in the response to cell-mediated immunity
1) APC presents the antigen on the surface of the cell
2) T helper cells have receptors which complement the antigen
3) when the t helper cell binds to the antigen, the t helper cell becomes activated (clonal selection)
4) They produce interleukins
5) this stimulates more T cells that are specific to the antigen to divide and form clones (clonal expansion)
6) the clones then do one of four things:
- produce interleukins to stimulate phagocytosis
- produce interleukins to stimulate B cells to divide
- differentiate into T killer cells
- differentiate into T memory cells
whats the difference between cell mediated immunity and humoral immunity
cell-mediated immunity - responses to cells that have been changed in some way
humoral immunity - response to antigens found outside of cells in body fluids (bacteria and fungi)
how does the body respond to humoral immunity?
1) B lymphocytes covered in antibodies bind to specific antigens (clonal selection) OR B lymphocytes engulfs the pathogen and present the antigen on the surface
2) With the help from the T helper cell interleukins, the B cells are activated and divide by clonal expansion
3) the clones develop into either plasma cells producing antibodies or into memory cells
what is the difference between the primary and secondary immune response
primary response - when the pathogen enters for the first time, you have a slow recovery, B and T lymphocytes are activated and you get symptoms
secondary response - when the pathogen enters for the 2nd time, fast recovery, memory cells are activated and you have no symptoms
What is active immunity
Memory cells are produced
Long term protection
Protection has to develop
Requires exposure to antigens
What is passive immunity
No memory cells produced
Short term protection
Immediate protection
No exposure to antigen
Give an example of:
- natural active immunity
- natural passive
- artificial active
- artificial passive
Natural active - secondary response to antigen entering the body for second time
Natural passive - antibodies from mother passing into baby in breast milk
Artificial active - vaccine with dead pathogens injected into person
Artificial passive - vaccine containing antibodies injected into person
How do vaccines work
A dead or inactive pathogen enters the body. It contains the antigens from the pathogen. Antibodies are produced by the white blood cells. These bind to the antigens of the vaccine. Memory cells now know the antigen so if the pathogen returns the body can produce the right white blood cells quickly to destroy the pathogen.
What is herd immunity
When a high percentage of the population is protected through a vaccine against a virus or bacteria which prevents the disease from spreading.
Protects people who can’t have the vaccine like children or ill people because the disease can’t spread.
define parasite
an organism which lives in or on another organism (its host) and benefits by deriving nutrients at the other’s expense
