Unit 4 - Communicable disease, disease prevention and the immune system Flashcards
Pathogen
Microorganism that causes disease
Lives in hosts
Communicable diseases
Any disease transmitted from one person or animal; contagious
4 groups of microorganisms
Bacteria
Fungi
Viruses
Protoctista
Diseases caused by bacteria
Tuberculosis
Bacterial meningitis
Ring rot in plants
Diseases caused by viruses
HIV/ AIDS
Influenza
Tobacco mosaic virus
Diseases caused by fungi
Black sigatoka
Ringworm
Athletes foot
Diseases caused by protoctista
Malaria
Potato/ tomato blight
Prokaryotic pathogens
Bacteria
Eukaryotic pathogens
Fungi
How do bacteria damage hosts
Multiply rapidly
Damage cells by releasing waste products and/or toxins
How do fungi damage hosts
Hyphae release extracellular enzymes e.g. celluloses to digest plant tissue
Causes decay and leaf death —> no photosynthesis
May produce toxins
Are viruses eukaryotic or prokaryotic
Neither; they’re dead
How do viruses damage hosts
Invade living cells where genetic material in virus takes over the biochemistry of the host cells
Makes more copies
Host cell bursts, releasing viruses
Bacteriophages
Viruses that can attack bacteria
How do protoctista damage hosts
Enter host cells and feed on contents before breaking over cells
How may protoctista enter through the body directly
Polluted water
Transmission
Passing a pathogen from an infected individual to an uninflected individual
Direct transmission
Passing a pathogen from host to new host, with no intermediary
Types of direct transmission
Physical contact
Faecal - oral transmission
Droplet infection
Transmission by spores
Physical contact
Touching an infected person
Touching contaminated surfaces
Exchanging bodily fluids
Faecal - oral transmission
Eating food or drinking water contaminated by pathogen
Droplet infection
Pathogens are carried in tiny water droplets in the air
Transmission by spores
Spores are the resistant stage of some pathogens
Can be carried in the air or reside on surfaces or in the soil
Indirect transmission
Pathogens are transmitted indirectly via a vector
Vector
Another organism that may be used by the pathogen to gain entry to the primary host
Cause of malaria
Plasmodium parasite
It enters the human host via a bite from a female Anopheles mosquito
Social factors affect direct transmission
Overcrowding Poor ventilation Poor sanitation Poor health - likely to contract other diseases Poor diet (malnutrition) Lack of education
Why is there a greater variety of diseases to be found in warmer climates
Many protoctists, bacteria and fungi can grow and reproduce more rapidly in warm and moist conditions
Why are plants targets for microorganisms
Manufacture sugars in photosynthesis and convert this into wide variety of compounds such as proteins and oils - rich source of nutrients for microorganisms
Passive defences
Prevent entry
Active defences
Induced when pathogen is detected
Plant passive defences
Cell wall Waxy cuticle Bark Stomatal closure Chemicals with anti pathogenic properties
Plant active defences
Production of callose Strengthen cell walls with additional cellulose and lignin Tylose formation Wide range of chemicals produced Necrosis
Callose as an active defence
Blocks plasmodesmata and sieve plates in the phloem, sealing off the infected part
Tylose
Ballon like swelling that fills the xylem vessel. When a tylose is fully formed it blocks the vessel
Necrosis as an active defence
Deliberate cell suicide
By killing cells surrounding the infections, pathogens access to water and nutrients is limited
Chemicals produced as a part of plants active defences
Terpenoids Phenols Alkaloids Defensins Hydrolysis enzymes
Terpenoids
Essential oils with anti-fungal and antibacterial properties
Phenols
Have antibiotic and anti-fungal properties
Tannins bind to salivary proteins and digestive enzymes, deactivating them
Alkaloids
Nitrogen-containing compounds that have a bitter taste to inhibit herbivores feeding
Inhibit protein synthesis
Also inhibit or activate enzyme action
Defensins
Small cysteine-rich proteins with anti-microbial properties
Act upon molecules in plasma membrane of pathogens
Hydrolytic enzymes
Found in spaces between cells
Include chitinases, glucanases and lysozymes
Glucanases
Hydrolyse glycosidic bonds in glucans
Primary Defences
Defences that prevent pathogens from entering the body
Non-specific defences
Prevent the entry of all pathogens
Primary non-specific responses
Blood clotting; vessels/skin receptor Expulsive reflexes Stomach acid Tears (enzymes break down e.g. bacterial cell wall) Wax in ears Mucous membranes Skin Inflammatory response
Main primary response
Skin
Cells in epidermis
Keratinocytes
How are keratinocytes produced
Cells produced at base by mitosis
Cells migrate to the top and keratinisation takes place
Keratinisation
Cytoplasm dries out and is replaced by keratin
Keratinised layer forms an effective barrier to pathogens
Where are mucous membranes found
In many of the body tracts that are at risk of infection as they are in contact with the external environment
What happens when mucus wafts to the top of the trachea
It enters the oesophagus and is swallowed. Most pathogens are killed by the acidity of the stomach
Examples of expulsive reflexes
Coughing
Sneezing
Vomiting
What are expulsive reflexes a result of
Irritation by micro-organisms or toxins in areas that are sensitive. The aim is to expel the microorganism
What happens when platelets come into contact with collagen in the skin or walls of damaged blood vessels
They adhere and begin secreting several substances including clotting factors and serotonin
Clotting factors
Thromboplastin
What does thromboplastin trigger
An enzyme cascade of reactions resulting in the formation of a blood clot. The final step is soluble fibrinogen being converted into insoluble fibrin fibres which forms a barrier
What does serotonin do
Makes the smooth muscle in the walls of the blood vessels contract, reducing supply of blood to the area
Inflammatory response
This is a localised response to pathogens resulting in inflammation at the site of a wound
Causes pain, heat, redness and tissue swelling
When mast cells are activated in damaged tissues, what chemicals are released from the cell
Histamines
Cytokines
Histamines
Makes arterioles dilate to increase blood flow (cause redness) and makes the capillary walls more leaky so more plasma is forced out. The extra tissue fluid causes oedema and pain
Oedema
Swelling
What do macrophages measure
Amount of bacteria entering the body
Roles of macrophages
Swallow pathogens and trap them in membranes
Breaks down pathogens by enzymes and kills them
Cause inflammation by ordering blood vessels to release water
Release interleukins
How long do neutrophils last
Only 5 days
Parasite
A microorganism that lives on a host and feeds on it
Causes harm to host
Secondary defences
Defences that combat pathogens once they have entered the body
How is it that we identify pathogens as foreign
All cells have antigens. Antigens not specific to the organism (self) are recognised as foreign
Antigens
Functional proteins/glycosidic proteins intrinsic to the plasma membrane
Opsonins
Opsonins are protein molecules (antibodies) that attach to the antigens on the surface of a pathogen and assist binding to phagocyte
Can be vey specific or not depending if they’re part of the non-specific response or specific response
Role of opsonins
Enhances the ability of phagocytic cells to bind and engulf the pathogen by acting as a marker
Phagocytes
Specialised cells in the blood and tissue fluid that engulf and digest pathogens (phagocytosis)
Examples of phagocytes
Neutrophils
Macrophages
Dendrites
Dendritic cells
Specialised forms of macrophages
Process of phagocytosis
Neutrophils bind to opsonins attached to antigen on pathogen
Pathogen engulfed (endocytosis) –> phagosomes
Lysosomes fuses with phagosome, releases hydrolytic enzymes (digestion)
After digestion harmless products are absorbed by the cell
When are neutrophils released in large numbers
During infection
When is pus formed
When neutrophils have collected in an area of infection
Antigen Presenting Cells (APCs)
Macrophages
Dendritic cells
How do cells become APCs
Larger cells manufactured in the bone marrow
Travel in the blood as monocytes before maturing into macrophages and dendritic cells
When pathogen is engulfed, it is not fully digested but instead saved and moved onto MHC proteins on the surface of the cell
MHC proteins
Special protein complex
What do MHC proteins ensure
That the APCs aren’t mistaken for a foreign cell and attacked by other pathogens
What happens when APCs move to the lymph node
The APC binds to the T cell with the correct receptors and activates to so it can start clonal selection
Where are dendritic cells found
In peripheral tissues
What are neutrophils attracted to
Monokines - type of cytokines (chemotaxis)
What do T helper cells release
Cytokines
These stimulate phagocytosis and B cells to develop
What do all T cells release
Interleukins (type of cytokines)
T killer cells
Attack and kill host-body cells that display the foreign antigen
What are T killer cells stimulated by
interferon
What do T memory cells provide
Long term immunity
Plasma cells
Develop from B cells
Circulate in the blood manufacturing & releasing antibodies
Produce antibodies that attach to antigens on pathogens and disable them
B memory cells
Develop from B cells
Remain in the body for a number of years & act as the neurological memory
If infected by the same pathogen again divide rapidly to form plasma cell clones
What does the specific immune response produce
Antibodies
Clonal expansion
Once activated the T-lymphocyte divides rapidly by mitosis
What do T-lymphocytes differentiate into
Mature T cells: T helper cells T killer cells T memory cells T regulator cells
T regulator cells
Shut down the immune response after the pathogen is removed. Involved in preventing autoimmunity
B cell activation
Activated T helper cells bind to B cells with matching BCR
Interleukins promote activation (clonal selection)
Activated B cells divides by mitosis (clonal expansion)
Cell mediated immunity
Refers to attacking infected host cells
What cells are most important in cell mediated immunity
T killer cells
Humoral immunity
important in attacking antigens outside of host cells e.g. bacteria and fungi
Humoral response
Produces plasma cells that produce antibodies
Cytokines
Chemicals that allow communication of cells in the immune system
What does interferon inhibit
Virus replication
Immunoglobulins
Complex proteins produced by plasma cells e.g. antibodies
Distinct regions of antibodies
Variable
Constant - same in all antibodies
Structure of antibodies
4 polypeptide chains (2 light and 2 heavy help together by disulphide bonds)
Which region of the antibody does the antigen bind to
Variable
Which region of the antibody does the phagocyte bind to
Constant
Main groups of antibodies
Opsonins
Agglutinins
Anti-toxins
Why are the opsonins in the specific response more effective than those in the non-specific response
They don’t bind tightly to specific antigens
Primary function of opsonins in the primary response
Promoting phagocytosis by acting as a marker
How do opsonins neutralise pathogens
If the antigen on the pathogen has a function (e.g. attachment to the host cell), the pathogen can no longer carry out this function
What can’t pathogens do when attached to antibodies
Enter host cells
Agglutinins
Because each antibody has two identical binding sites they can bind to several pathogens and crosslink them
When many antibodies perform this cross linking, pathogens become agglutinated
Agglutinated pathogens are …
Physically impeded from carrying out functions (neutralised)
Readily engulfed by phagocytes
Non-infective
Toxin
Protein that harms us
Antitoxins
Bind to toxins released by pathogenic cells. The actions of antitoxins renders them harmless
Primary immune response
Immune response when a pathogen is encountered for the first time
How long does it take for the no. of antibodies in the blood to rise
5 days for everything to occur (e.g. phagocytosis, APCs, migration to lymph, T &B clonal selection and expansion)
In the meantime, pathogens multiply and we experience symptoms
Secondary immune response
T and B memory cells circulating in blood are rapidly activated if the pathogens infect again
V. quick production of antibodies for higher conc. and sustained for longer
Pathogen is killed before we notice symptoms
When do autoimmune diseases occur
When the immune system recognises a ‘self’ antigen as a foreign antigen & attacks healthy body tissue
Immunity
Being able to kill pathogens if infected before getting symptoms
-ve of immunosuppressants
May deprive the body of its natural defence against pathogens
Active immunity
Achieved when immune system is activated and manufactures its own antibodies
Passive immunity
Achieved when antibodies are supplied from another source
Natural immunity
Achieved through normal life processes
Artificial immunity
Achieved through medical intervention
Natural active immunity
Achieved as a result of infection
Active artificial immunity
Achieved as a result of vaccination
Passive natural immunity
Antibodies provided via the placenta or via breast milk
Passive artificial immunity
Provided by infection of antibodies made by another individual
Vaccinations
Deliberately exposing the body to antigenic material to trigger long-term immunity (through activation of the specific immune response leading to memory cells)
Types of antigenic material
Whole live organisms that aren’t as harmful as ones causing the disease but have same antigens - cowpox for smallpox virus
Harmless or attenuated - Measles
Dead pathogen - cholera
Antigens from the pathogen - Hepatitis B
Toxoid - Tetanus
Toxoid
Harmless version of a toxin
Attenuated
Weakened
Herd vaccinations
Using a vaccine that provides immunity to all/nearly all at risk. To achieve this 80-95% of the population has to be vaccinated
Ring vaccination
Used when new case of disease is reported
Only those in immediate vicinity are vaccinated
When do epidemics rise
When some pathogens undergo genetic mutations which change their antigens so the memory cells may not remember them
Pandemics
Worldwide epidemics
How are pandemics avoided
Epidemics are closely monitored on a global level so that new strains can be identified and controlled
Source of penicillin
Penicillium
Source of morphine
Unripe poppy seeds
Source of aspirin
Willow-bark extract
Why do we still need new drugs
New diseases emerging
Many diseases w/ no effective treatments
Some antibiotic treatments are becoming ineffective
Why is it important to maintain biodiversity in terms of medicines
To make sure we don’t destroy a plant, animal or microorganisms which could give us a life-saving drug
Personalised medicines
Once gene sequencing technology is fully developed it will be possible to sequence the genes from individuals with particular conditions and develop specific drugs fro their condition
Pharmacogenomics
The science of interweaving knowledge of drug actions with personal genetic material
Synthetic biology
We can genetically modify microorganisms or plants to contain a gene that produces a beneficial protein e.g. bacteria are modified to produce human insulin
Antibiotics
Drugs that interfere with the metabolism of bacteria without the metabolism of human cells - selective toxicity
Polymixines
Makes holes in bacterium cell membrane –> altering permeability
Penicillin and cephalosporins
Weaken the peptidoglycan cell wall so bacterium can be more easily damaged by immune system
Why is antibiotic resistance growing
Overusing antibiotics in both the health sector (prescribing when unnecessary) in meat industry
How does antibiotic resistance develop
Random mutation Selection pressure (adding antibiotics) Those with mutations that allow resistance survive & reproduce, others die Next generation has more individuals with the characteristic (resistance)
Examples of resistance
MRSA (Methicillin-resistant Staphylococcus aureus)
Clostridium difficile
What can we do about antibiotic resistance
Promote good hygiene in hospitals, care homes and in general prevent spread of resistant strains
Use new, innovative ways of developing antibiotics (computer modelling and/or looking for new sources of medicine in unusual places)
Educate public and healthcare professionals to minimise use of antibiotics and ensure all courses of antibiotics are completed
Lymphocyte involved in cell mediated response
T cells
Lymphocytes involves in humoral response
B cells
What are interleukins used for
Cell signalling in the specific immune response
Blood smear analysis
Most cells are RBC as they have no nucleus
Darker cells are neutrophils
Types of cytokines
Monokines - attract neutrophils
Interleukins - released by t helper cells and activate B cells
Why may some people experience discomfort in their armpits after an infection
Excess tissue fluid drained to lymph nodes
Pathogens in tissue fluid enter lymph
B effector cells
B lymphocytes that divide to form plasma cell clones
