communicable disease- can be passed from one organism to another of the same or different species
pathogen - microorganism that causes disease. includes bacteria, fungi, viruses and protoctista
vectors - a living or non-living factor that transmits a pathogen from one organism to another
Bacteria:
rod shaped - bacilli
spherical - cocci
comma shaped - vibrios
spiralled - spirilla
corkscrew - spirochaetes
Bacteria cell wall:
there are two different types of bacterial cell wall that are identified by gram staining
gram staining is a method of staining bacteria using a dye called crystal violet
the gram-staining characteristics of bacteria are denoted as positive or negative depending on whether they take up the stain
gram positive bacteria look purple-blue under the light microscope e.g. MRSA
gram negative bacteria appear red under a light microscope e.g. E. Coli
Viruses:
non-living infectious agents
0.02-0.3 micrometers in diameter - 50x smaller than bacteria
DNA or RNA surrounded by a protein coat
Viruses invade living cells. the genetic material in the virus will take over the very biochemistry of the cell and use it to produce more viruses
all naturally occurring viruses are pathogens
Bacteriophages: viruses that attack bacteria, used for scientific research to identify and treat diseases
Protoctista:
eukaryotic organisms
include single cell organisms and cells grouped into colonies `
some protista are pathogenic
e.g. malaria, sleeping sickness, amoebic dysentery and giardia
Fungi:
Eukaryotic single and multicellular organisms
causes irritation in animals
most fungi are saprophytes, but some are parasitic
fungal affections often affect leaves
fungi reproduce by spores which can spread quickly
Viruses - damage
take over cell metabolism
insert viral genetic material into host DNA
uses host cell to make more viruses which then burst out of the cell
destroys the cell and viruses go on to infect more cells
Protoctista - damage:
take over cell and digest its components
do not take over genetic material
break open and destroy cells as new generation emerges
Fungi - damage:
digest and destroy living cells as food
symptoms stem from this process and body reponse
may also produce toxins which affect the host
Bacteria - damage:
enter cells or live on surface
produce toxins that are a by-product of the normal functions of the bacterial cell
toxins cause:
damage to cell membranes
interference with host cell's genetic material
damage or inactivation of enzymes
Plant defences against pathogens:
waxy cuticle
bark on trees
cellulose cell walls
sacrifice infected area by shutting it off
When a plant is attacked:
receptors in the cell responds to molecules from the pathogens or to chemicals produced when the plant cell wall is attacked
this stimulates signaling molecules to be released (e.g. nitric oxide) which causes genes to be switched on in the nucleus . This then triggers cell responses such as:
produce defensive chemicals
produce chemicals that send an alarm signal to unaffected cells to trigger their defences
produce the polysaccharides callose and lignin to strengthen the cell wall
Plant physical defences:
when a plant is attacked, it produces high levels of the polysaccharide callose
callose has beta-1,3 linkages and beta-1,6 linkages
callose is placed between the cell walls and the cell membranes of cells next to infected cells, acting as a barrier against the pathogen
lignin is added, and callose blocks sieve plates in the phloem to seal off the infected area
callose is deposited in the plasmodesmata, sealing infected cells off from healthy cells
Plant Chemical Defences:
plants produce powerful chemicals to repel insect vectors or kill invading pathogens:
the skin has a flora of healthy microorganisms that outcompete pathogens for space
skin produces sebum, this is an oily substance that inhibits the growth of pathogens
Mucous membranes:
e.g. found in the airways
secrete sticky mucus
microorganisms get stuck in the mucus
mucus contains lysozymes that destroy bacterial and fungal cell walls
mucus contains phagocytes
Lysozymes/acid:
antimicrobial enzymes found in tears and urine
acid found in stomach; low ph denatures proteins
Expulsive reflexes:
coughing and sneezing expels pathogen-laden mucus from airways
vomiting and diarrhoea expels contents of the gut
Blood clotting:
platelets come into contact with collagen and adhere to surfaces
they release thromboplastin which catalyses prothrombin to turn into thrombin
thrombin catalyses fibrinogen to turn into fibrin which forms the clot
Serotonin:
causes smooth muscle to contract, narrowing blood vessels and reducing blood supply to wounded area
Scabbing:
once the clot has formed, it will dry out and prevent pathogens entering
epidermal cells begin to grow below the scab
blood vessels regrow
collagen fibres are deposited to give the tissue strength
the scab will slough off and the wound is healed
Inflammatory response:
localised response to pathogens resulting in inflammation, characterised by pain, heat, redness and swelling
when tissues are damaged, mast cells are activated and release chemicals such as histamines and cytokines to attract phagocytes or make blood vessels dilate/leak
Phagocytosis:
phagocyte attracted by chemicals produced by pathogen
phagocyte recognises pathogen as non-self and binds to it
phagocyte engulfs pathogen to form phagosome; lysosome moves towards phagosome and combines with it, forming phagolysosome
enzymes break down pathogen
digested pathogen absorbed by phagocyte; antigens combine with major histocompatibility complex in cytoplasm
MHC/antigen complex is displayed on phagocyte, making it an APC
Fevers:
normal body temp: 37 degrees, controlled by hypothalamus
cytokines stimulate hypothalamus to increase body temperature
higher temperatures inhibit pathogen reproduction
specific immune system works faster
Phagocytes:
build up at the site of infection, forming pus
neutrophils and macrophages
neutrophils do not form APCs but macrophages do
Cytokines:
produced by phagocytes
act as cell-signalling molecules and inform other cells that the body is under attack
also stimulate specific immune response and increase body temperature
Opsonins:
enhance phagocytosis by marking antigen for immune response
receptors on phagocytes will bind to common opsonins, helping the phagocyte engulf that pathogen
antibodies such as IgG and IgM are strong opsonins
Antigens:
molecules found on the surface of all cells
body recognises difference between self-antigens and non-self antigens
toxins also act as antigens
Antibodies:
Y shaped glycoproteins called immunglobulins
bind to specific antigens on pathogen/toxin
each one is specific to an antigen
can act as opsonins
made up of 4 identical polypeptide chains, two long (heavy) and two short (light)
held together by disulfide bridges
binding site made of 110 amino acids - variable region
lock and key mechanism
Antibodies are produced by B plasma cells and can:
act as an opsonin
bind to antigens to prevent them entering other cells
act as agglutinins
act as anti-toxins
T helper cells:
have CD4 receptors on membrane which bind to the antigens on APCs
produce interleukins which stimulate B cells to produce antibodies, other T cells to be produced, macrophages to ingest pathogens
T killer cells:
destroy the pathogen with the antigen on its surface or infected body cells
use perforin to make holes in pathogenic membranes
T memory cells:
part of immunological memory
divide rapidly when exposed to a pathogen to form T killer and T helper cells
T regulator cells:
suppress the immune system
stop an immune response once a pathogen has been eliminated
ensure body recognises its own antigens and doesn't set up an autoimmune response
B effector cells:
divide to produce plasma cells
B Plasma cells:
produce antibodies for a specific pathogen and release them into circulation
only live for a few days but release 2000 antibodies per second
B memory cells:
part of immunological memory
will recognise antigens they've seen before
allows for a rapid secondary immune response
Cell-mediated immunity:
macrophages digest pathogen
antigens are processed and placed on macrophage surface
T helper cell complimentary to antigen binds to macrophage and becomes activated
activated t helper cell releases interleukins which stimulate other T cells to divide into memory cells, produce interleukins for phagocytosis, cause B plasma cells to divide, develop into T Killer Cells