Module 4.1 Communicable Diseases Flashcards
Pathogen
Microorganisms that cause disease
4 types of pathogens
- Bacteria (prokaryotes)
- Fungi
- Viruses
- Protoctista e.g. malaria
Bacteria/prokaryotes
-Smaller than eukaryotes
-Reproduce rapidly
-Damage cells through release of toxins
E.g. TB and ring rot
Fungi
-Often live in skin
-Hyphae form a mycelium
-Reproductive hyphae grow in the skin and release spores
-In plants, they live in vascular tissue to gain nutrients
-Hyphae release extracellular digestive enzymes to break down cellulose which decays the plant
E.g. Black sigatoka (bananas), ringworm (cattle) and athlete’s foot
Protoctista
-Enter host cell and feed on cell contents
E.g. Malaria parasite (plasmodium) has immature forms that feed on haemoglobin (mosquitos are the vector), potato/tomato late blight
Viruses
-Invade cells then take over genetic machinery and other organelles
-Causes the cell to manufacture more copies of the virus
-Host cell eventually bursts, releasing new viruses to invade new host cells
E.g. HIV, influenza, tobacco mosaic virus
Direct transfer
- Physical contact
- Faecal-oral transmission
- Droplet infection
- Spore transmission
Indirect transfer
- Transmission via vectors e.g. Malaria via mosquitos
- Vehicles (not living things) e.g. Chopping board
Factors which affect disease transmission
- Hygiene
- Food prep.
- Sewage treatment
- Poor health
- Poor diet
- Human migration
- Overcrowding
- Homelessness
- Poor ventilation
Transmission of plant pathogens
-Direct or indirect
-Usually through roots
-Airbourne transmission of spores
-Once the pathogen has infected all vascular tissue and the leaves shed, it will spread to the soil and infect other plants
-Indirect transfer e.g. spores attach to an insect and are then transferred
E.g. Dutch Elm disease
Passive defences in plants
- Cellulose cell wall provides a physical barrier
- Waxy cuticle - physical barrier - prevents water containing pathogens collecting
- Bark - physical barrier and contains chemicals that will work against pathogens
- Tylose formation - physical barrier - balloon like projection, fills the xylem, acts as a plug, prevents the xylem from carrying water which prevents the spread of pathogens - also chemical barrier - contains lots of terpenes (toxic to many pathogens)
- Callose - physical barrier - large polysaccharide deposited within sieve tube when a pathogen is detected - blocks flow in sieve tube element and plasmodesmata preventing the spread of the pathogen
Active defences in plants
- Cellulose cell wall (can thicken w more cellulose)
- Callose deposition
- Oxidative bursts - produce highly reactive oxygen molecules which damage the pathogen
- Necrosis (deliberate death of infected cells)
- More chemicals produced
Non-specific primary defences
- Skin - keratin coats the epidermis
- Blood clotting
- Mucous membranes
- Wax in ear canal
- Tears containing lysozyme
- Coughing, sneezing and vomiting
- Amylase in saliva
- HCl in the stomach
- Cilia on the ciliated epithelium in the trachea/airways
- Mucous plug in the cervix
Expulsive reflexes examples
Coughing, sneezing and vomiting
How inflammation occurs
- Microbes detected by mast cells which release histamine
- Release of histamine causes vasodilation meaning the capillaries are more permeable so more WBCs can leave
- More tissue fluid forms because more plasma leaves
- Causes oedema
- Tissue fluid can drain into the lymph vessels so pathogens may come into contact w lymphocytes and trigger a specific immune response
Why is it important that the blood clots?
- To prevent pathogens getting in
- To prevent blood loss
The process of blood clotting and skin repair
- Blood vessel damaged - platelets bind to exposed collagen to form a temporary platelet plug
- Platelets also release clotting factors which activate an enzyme cascade
- Enzymes cause fibrinogen to form insoluble fibres which attach to the plug
- RBCs trapped - clot forms
- The clot dries and forms a scab which pulls the skin closer together
- Under the skin, collagen is deposited
- Stem cells in the epidermis divide by mitosis and differentiation occurs to form new skin cells at the edge of the cut
- Blood vessel gets repaired
- When the edges of the cut are drawn together the repair is complete
3 types of phagocyte
- Neutrophils
- Macrophages
- Antigen presenting cells
Antigens
- Proteins found on cell surface membranes
- Antigens are specific to each individual so antigens on pathogens will be recognised as foreign and produce a response
Opsonins
- Type of antibody (protein) which attaches to antigens on cell surface membranes
- Not very specific
- Makes it easier for phagocyte to bind to and engulf pathogens
Neutrophils
- Most common phagocyte
- Made in bone marrow
- Travel in blood
- Can pass into tissue fluid - slightly flexible, can fit through gaps in endothelium
🌟Phagocytosis process
- Opsonin binds to antigen on pathogen’s cell surface membrane
- Receptor on neutrophil’s cell surface membrane binds to opsonin
- Pathogen engulfed by endocytosis
- Phagosome produced
- Lysosomes fuse w the phagosome
- Lytic enzymes are released
- Pathogen digested into amino acids and fatty acids
- Products absorbed into cytoplasm by diffusion
Macrophages
- Made in bone marrow
- Travel in blood as monocytes
- Settle in lymph nodes and mature to macrophages
- Initiate immune response
Macrophages –> antigen presenting cells
- When macrophages engulf pathogens, they aren’t completely digested
- They separate the pathogen’s antigens and incorporate them into their own cell surface membrane
- They are now antigen presenting cells and they increase the chance of the correct T lymphocytes locating the foreign antigens
How to recognise RBCs on a micrograph
- Majority of cells
- Pink/red
How to recognise neutrophils on a micrograph
-Multilobed nucleus
How to recognise monocytes on a micrograph
- Largest WBC
- Large, kidney shaped nucleus
How to recognise lymphocytes on a micrograph
- Smaller
- Nuclei almost fill cell
Why is there a delay between the first infection by the pathogen and the appearance of antibodies in the blood?
- Time taken for clonal selection
- Time taken for clonal expansion
- Time taken for antigen presentation
- Time taken for differentiation
- Production of antibodies takes time
- No memory cells
What type of cell matures in the thymus?
T lymphocytes
What type of cell secretes substances which kill infected cells?
T killer cells
What type of cell makes antibodies?
Plasma cells
What types of cells undergo clonal expansion?
B and T lymphocytes
What type of cell activates other lymphocytes?
T helper cells
Outline how the structure of an antibody molecule relates to its function
- Constant region - for binding to receptors on phagocytes
- Variable region - complimentary in shape to the antigen, binds to it
- Hinge region- flexibility of branches - can bind to more than 1 antigen
- Disulfide bonds - tertiary structure
Describe how antibodies act on invading pathogens
- Variable region binds to antigen
- Variable region specific to antigen
- Opsonins cause neutralisation of pathogens as antibodies cover the binding sites on pathogens preventing entry to the host cell
- Multiple variable regions allow antibodies to agglutinate many pathogens together, preventing them from entering the host cell and increasing the likelihood of phagocytosis
Describe the action of phagocytic cells at sites of infection
- Pathogen recognised as foreign
- Endocytosis
- Phagosome produced
- Lysosomes fuse w the phagosome and lyctic enzymes are released
- The pathogen is digested/pathogen hydrolysed
Describe the changes that occur to T lymphocytes during an immune response and explain the role of T lymphocytes in fighting a infection by a pathogen
- Antigens presented
- Receptors on T lymphocytes complimentary and specific to antigen
- Clonal selection
- Clonal expansion
- Mitosis
- T helper cells - release interleukins w specific shapes which bind to complimentary receptors on the cell surface membrane of B lymphocytes, stimulating them to divide by mitosis and differentiate, they also stimulate macrophages to carry out more phagocytosis
- T killer cells - search for and kill infected host cells displaying foreign antigens by secreting protease enzymes
- T memory cells - stay in blood in case of a second invasion, provide active immunity, allow faster secondary response, recognise antigen and can make clones and change to form new T cells more quickly than in the primary response
- T regulator cells - stop immune response once pathogen removed, preventing autoimmunity
Triggering a specific immune response
- Antigens on the pathogen’s surface communicate to our body’s cells that it is foreign
- To initiate an immune response, the pathogens have to be detected by B and T lymphocytes w the correct complimentary receptors to the pathogen’s antigens
- Infected cells sometimes get the pathogen’s antigens on their surfaces which helps select the right B and T lymphocytes
- Macrophages in the lymph nodes engulf and digest pathogens, incorporating their antigens onto their own cell surface membrane –> they are now antigen presenting cells - they inc. the chances of the correct T lymphocytes locating the foreign antigens
- The selection of the correct lymphocytes w receptors complimentary in shape to the antigen = clonal selection
- More of these lymphocytes are needed to fight the pathogens so they divide by mitosis in clonal expansion
T helper cells
Release interleukins w specific shapes which bind to complimentary receptors on the cell surface membrane of B lymphocytes, stimulating them to divide by mitosis and differentiate. They also stimulate macrophages to carry out more phagocytosis
T killer cells
Search for and kill infected host cells displaying foreign antigens by secreting protease enzymes into them
T memory cells
Stay in blood in case of a second invasion by the same pathogen - provide immunity. They allow a faster secondary response because they recognise the antigen and can make clones and change to form new T cells more quickly than in the primary response
T regulator cells
Stop immune response after the pathogen has been removed, preventing autoimmunity
Plasma cells
Produce and secrets antibodies which are complimentary in shape to the antigen
B memory cells
Stay in the blood in case there is a second invasion by the same pathogen. They allow a faster secondary response because they recognise the antigen and can make clones and change to form new plasma cells and so antibodies are made more quickly than in the primary response.
🌟Examples of cell signalling in the immune response
- Pathogen’s antigens communicate to body cells that they are foreign
- Infected cells w foreign antigens on the surface communicate to lymphocytes to be selected in clonal selection and to T killer cells that they need to be killed
- Antigen presenting cells communicate to T lymphocytes to be selected in clonal selection
- Macrophages release monokines which attract neutrophils and stimulate B lymphocytes to differentiate into plasma cells
- T helper cells release interleukins which bind to receptors on B lymphocytes and stimulate them to divide by mitosis and differentiate
🌟Describe and explain the primary and secondary immune responses
Primary response:
- Time delay to trigger the immune response after the first infection
- No B memory cells - slow antibody production and few produced
Secondary response:
- Shorter delay before response
- Response much quicker
- B memory cells specific to antigen of the pathogen have remained in the blood after being produced in the primary response. They can clone and differentiate to make plasma cells which make more antibodies much more quickly. They give immunity to a disease
🌟The structure of antibodies and how this relates to their function
4 polypeptide chains, 2 light, 2 heavy, disulfide bonds, Y shaped
- Constant region - for binding to phagocytes
- Variable region - complimentary in shape to the antigen so it binds to it
- More than 1 variable region - allows attachment to more than 1 antigen (hence attaching to more than 1 pathogen –> agglutination)
- Hinge region - allows flexibility of branches so they can move closer or further apart to bind to more than 1 antigen
Opsonins
- Antibodies which bind to antigens on pathogens
- Receptors on neutrophils’ cell surface membrane bind to opsonins (constant region)
- Pathogens are engulfed by endocytosis
- Some opsonins are specific
- Some aren’t specific and bind to peptidoglycan/murein
- Opsonins cause neutralisation of pathogens because antibodies cover the binding sites on pathogens which prevents their entry to the host cell
Agglutinins
- Antibodies which cause agglutination of pathogens
- Multiple variable regions allow antibodies to clump/agglutinate together many pathogens
- The clump is too large to enter the host cell and increases the likelihood of being consumed by phagocytes
Antitoxins
-Antibodies which bind to the toxins produced by the pathogen which makes them harmless
Finding new drugs: microorganisms
-Antibiotics are produced naturally by microbes
E.g. The fungus penicillium makes the antibiotic penicillin
Finding new drugs: Plants
- Morphine came from the sap of a poppy originally
- Willow bark extract led to the development of aspirin and ibuprofen
- They isolate the active ingredient then work out how to make it synthetically
Personalised medicines
By sequencing genomes, scientists may be able to develop drugs for specific conditions
Synthetic biology
-Development of new molecules e.g. enzymes that mimic natural processes/use natural molecules to produce new biological systems that don’t exist in nature
E.g. Introducing anthocyanin in tomatoes to protect against CHD
Benefits of using antibiotics
- Prevent post surgery infection
- Treat infections that the body can’t fight off
Downsides to using antibiotics to treat infections
Overuse/misuse can lead to resistant strains of bacteria
History of antibiotics
- During WW2, antibiotics were used readily to prevent infection
- Overuse/misuse led to resistance
MRSA and clostridium difficule
- Both particularly resistant strains of bacteria
- Infections v hard to treat and are particularly dangerous for people w weakened immune systems
Why is the term “immune” incorrect when referring to bacteria and antibiotics?
- Resistant is the correct term
- Immune implies they have an immune system which they don’t as they are single felled organisms
🌟Groups that should be immunised
- Elderly (weak immune system)
- Young children (have had little time to build up natural immunity)
- HIV/AIDS victims
- Pregnant women
- Health workers
- People w TB or an autoimmune disease
- People living in close proximity to an outbreak
What antigenic material could be used in a vaccine?
- Antigens
- A harmless or dead version of the pathogen
- Microbes w similar shaped antigens
🌟Herd/Routine vaccination
-Vaccinate all people at risk
-When enough people are immune it stops disease spreading
E.g. The UK MMR vaccination programme
🌟Ring vaccination
- Requires people to report victims
- You vaccinate all people living w or near the victim
- Contains spread within the ring
Natural immunity
Gained in the normal course of living
Artificial immunity
Gained by deliberate exposure to antibodies and antigens
Passive immunity
Acquired without activation of lymphocytes - involves antibodies that aren’t your own e.g. Breastfeeding and across the placenta
Active immunity
Your immune system producing the antibodies
Example of natural active immunity
Previously having chicken pox
Example of artificial active immunity
Infection of weakened version of disease e.g. Influenza vaccine
Examples of natural passive immunity
- Across the placenta
- Breast milk
Example of artificial passive immunity
Infection of antibodies e.g. Tetanus vaccine
Reasons for changing vaccines and vaccine programmes
- If a disease is eradicated why waste money on vaccinations
- Stockpiling for outbreak
- Routine vaccinations need to be changed each year for diseases caused by quickly mutating pathogens e.g influenza
- Vaccinating all people at risk helps avoid epidemics/pandemics for new strains of disease
🌟Why are the elderly and young children advised to get an influenza vaccine yearly?
- Vaccine changes each year
- Mutations cause different strains of the virus each year
- New strains have different antigens
- The vaccine encourages new antibodies to be made
🌟Why do some people choose not to get immunised even though the government advise it?
- Too busy
- Can’t be bothered
- Media scare stories
- Side effects
- Allergic to vaccine
- Fear of needles
- Religious reasons
- Possibly cost
🌟Why do governments want people to be vaccinated (aside from the direct health benefits)?
- Prevents lost days at work which harms the economy
- Costs less to immunise people than to treat them
- Health service can’t cope w many people getting ill at once
🌟Malaria
- Caused by the protoctist plasmodium vivax
- Carried by the female anopheles mosquito (vector)
- Can also be transmitted by blood transfusions and across the placenta
🌟Malaria - life cycle
- A person w malaria has the gametes of P. vivax in the blood
- Person bitten by a female Anopheles mosquito
- Gametes in the blood go into its stomach
- Gametes fuse and zygotes of P. vivax develop in stomach
- These develop into infective stages and migrate salivary glands of mosquito
- The mosquito bites an uninfected person and insects some of its saliva containing infective P. vivax
- Infective stages of P. vivax enter new host’s liver and divide by mitosis
- These enter the blood and feed on haemoglobin in RBCs and make more gametes in the process
🌟HIV (human immunodeficiency virus)
AIDS (acquired immune deficiency disease)
- HIV causes AIDS
- HIV + = inactive version of virus present (no symptoms of AIDS) - can go unknown for a long time (during which time it can be transmitted)
- Active version of virus destroys T helper cells
- Lower ability to destroy pathogens
- Increases likelihood of contracting AIDS related diseases e.g. pneumonia
✨Why are rates of HIV/AIDS higher in sub-Saharan Africa than in the rest of the world?
- Poverty
- Less educated
- More promiscuity/ sex workers?
- Lower availability of condoms
- Religious reasons for not wearing condoms
- Denial of existence
- Fewer medical facilities for screening
- Less screening of blood for transfusion
- Infected mothers having to breast feed - no alternative
- More cases of rape
- More intravenous drug abuse
- More use of shared needles
✨TB
- Caused by the bacteria Mycobacterium tuberculosis and M. bovis
- Transmitted by droplet infection (droplets from coughs and sneezes being inhaled)
- Usually found in lungs
- Can be transmitted through milk or meat of infected cattle
Transmission more likely if..
- Overcrowding
- Poor ventilation
- Poor health
- Poor diet
- Homelessness
- Living/working w people who have migrated from areas w high prevalence of TB
✨Why TB hasn’t been eradicated
- LEDCs can’t afford vaccines/antibiotics
- Vaccine not 100% effective
- Antibiotic resistance
- People not finishing courses of antibiotics
- Lack of education about TB
- Drinking unpasteurised milk
- Migration of carriers (won’t experience symptoms)
🌟The role of antibodies
- Antibodies bind to antigens on pathogens
- Neutralisation of pathogens
- Antibodies cover the binding sites on pathogens - preventing entry into host cells
- Agglutination of pathogens
- Multiple variable regions allow antibodies to clump/agglutinate many pathogens together - clump too large to enter host cell and inc. likelihood of being consumed by phagocyte
🌟Immune response - T lymphocytes (cellular response)
- Macrophages engulf and digest pathogens - incorporate pathogen’ antigens into their own cell surface membrane –> now antigen presenting cells - this helps to select the right T lymphocytes w receptors complimentary in shape to the antigen = clonal selection
- Once the correct T lymphocytes are selected, they divide by mitosis = clonal expansion
- T helper cells - release cytokines w specific shapes which bind to complimentary receptors on the cell surface membranes of B lymphocytes, stimulating them to divide by mitosis and differentiate. They also stimulate macrophages to carry out more phagocytosis
- T killer cells - kill infected host cells by secreting protease enzymes into them
- T memory cells - stay in blood in case of 2nd invasion by same pathogen - allow faster secondary response because they recognise the antigen and can make clones and differentiate to form new T cells more quickly than in the primary response
🌟The changes and roles of B lymphocytes in an immune response (humoral response)
- Specific B lymphocytes w receptors complimentary in shape to the antigens on the invading pathogen are selected = clonal selection
- Cytokines released by T helper cells stimulate B lymphocytes to divide by mitosis in clonal expansion and then to differentiate into plasma cells and B memory cells
- Plasma cells - produce and secrete antibodies which are complimentary in shape to the antigen. These can cause agglutination or neutralisation of pathogens
- B memory cells - stay in blood in case of a second infection by the same pathogen - allows a faster secondary response because they recognise the antigen and can make clones and change to form new plasma cells and so antibodies are made more quickly than in the primary response
🌟Why has it not been possible to produce an effective vaccine for malaria?
- Different strains of the protoctist each year due to mutations
- New strains have different antigens
- More than one stage in its life cycle and different stages have different antigens and would require different vaccines
- The plasmodium is concealed in liver cells and the RBCs so it is only exposed to the immune system for a short period of time
