Communicable Diseases Flashcards
(126 cards)
1
Q
Communicable diseases?
A
Diseases that can be passed from one organism to another, of the same or different species
2
Q
What are pathogens?
A
Infective microorganism which cause disease
3
Q
Pathogens include?
A
Viruses, fungi, bacteria and protoctista - each with their own characteristics
4
Q
Communicable diseasess?
A
Animals they are most commonly spread from one individual of a species to another (intra) but they can also be spread between species (inter)
In plants they are spread directly from plant to plant
Vectors carry pathogens from one organism to another - common vectors include water and insects
5
Q
Bacteria
A
Small proportion of them are pathogenic and cause communicable diseases
They are PROKARYOTES so their cell structure is very different from eukaryotic organisms they infect - no membrane bound nucleus/organelles
6
Q
How can bacteria be classified?
A
By their basic shape rod shaped (bacilli), spherical (cocci), comma shaped (vibrios), spiralled (spirilla) and corkscrew (spirochaetes)
By their cell walls - two main types react differently to the process of gram staining ; gram positive bacteria look purple-blue under the light microscope but gram negative bacteria appear red (counter stain of safronin is applied) - this can be used to identify how bacteria react to different antibiotics
7
Q
Gram staining
A
Crystal violet and iodine is applied to fix the dye
Then is washed with alcohol (penetrates the cell walls and allows the violet-iodine complex to leak out) - gram positive bacteria retain the violet stain and appear blue/purple while gram negative bacteria have thinner cell walls so they lose the stain and they appear red (counterstain applied)
Gram positive bacteria are susceptible to penicillin which inhibits the formation of cell walls while gram negative bacteria have much thinner cell walls so are not susceptible to penicillin
8
Q
Viruses?
A
Non-living infectious agents and 50 times smaller in length than the average bacterium - basic structure is just some genetic material surrounded by a protein
They invade living cells where the genetic material takes over the host cell to make more viruses - reproduce rapidly and evolve rapidly too
They are all pathogenic and cause disease in every other type of organism
9
Q
What are bacteriophages!
A
Viruses that attack bacteria - use bacterial cells to replicate and destroy the bacteria at the same time ; used to identify and treat some diseases and they are very important in scientific research - PARASITES
10
Q
Protoctista
A
A group of eukaryotic organisms with a wide variety of feeding methods - they include single-celled organisms and cells grouped into colonies. A small percentage of protoctista act as pathogens, causing devastating communicable diseases in plants and animals - these are parasitic and use animals as their host organism ; they need a vector to transfer them to their hosts (malaria - mosquitoes) or they can enter through polluted water - amoebic dysentery
11
Q
Fungi
A
Eukaryotic organisms that are often multicellular (although yeasts are single celled) - fungi cannot photosynthesise and they digest their food extracellularly before absorbing the nutrients. Many fungi are saprophytes which means they feed in dead and decaying matter - however some fungi are parasitic, feeding on living plants and animals ; these are the pathogenic fungi which cause communicable diseases
Fungal diseases on plants affect the leaves, preventing photosynthesis and so quickly kill the plant - when fungi reproduce they produce millions of tiny spores which can spread long distances (they can spread rapidly through crops) - cause starvation
12
Q
How do pathogens damage host tissues directly?
A
Symptoms are caused by the damage pathogens do to tissues + the way in which the body of the host responds to the damage
13
Q
How do viruses damage host tissue?
A
Take over the cell metabolism - viral genetic material gets into the host cell and is inserted into the host DNA ; virus then uses the host cell to make new viruses which burst out of the cell, destroying it and spreading to infect other cells
14
Q
How to Protista take over cells?
A
They digest the cell and use the cell contents to reproduce (breaking open the cell) ; proctists which cause malaria are an example of this
15
Q
How else can pathogens damage host tissues?
A
Produce toxins - most bacteria produce toxins that poison or damage the host cells in some way, causing disease. Some bacterial toxins damage the host cells by breaking down the cell membranes, some damage/inactivate enzymes and some interfere with the host cell genetic material so they cells cannot divide
Some fungi produce toxins which affect host cells and cause disease
16
Q
Plant diseases repercussions
A
Cause starvation, economies may struggle and jobs lost - threaten ecosystems and entire species too
17
Q
Ring rot
A
Bacterial disease of potatoes, tomatoes and aubergines chased by gram positive bacteria Clavibacter - damages leaves, tubers and fruit with no cure. Once bacterial ring rot infects a field it cannot be used to grow potatoes again for at least 2 years
18
Q
Tobacco Mosaic Virus?
A
Virus that infects tobacco plants and 150 other species (tomatoes and peppers). Damages leaves, flowers and fruit and stunts growth - this reduces yields and can lead to total crop loss. Resistance crop stains are available but there is no cure
19
Q
Potato blight (think Ireland)
A
Fungus like protoctista oomycete Infestans - hyphae penetrate host cells, destroying leaves and tubers and fruit - no cure but resistant strains and chemical treatments can reduce infection risk
20
Q
Black Sigatoka
A
CAUSED BY FUNGUS
Attacks and destroys leaves
Hyphae penetrate and digest the cells - turning leaves black, if plants are infected it can reduce yield by 50% and resistant strains are being developed - fungicide (chemical that kills fungi) treatment can control the spread of the disease but there is no cure
21
Q
Food security
A
Plant diseases threaten staple crops like rice - threatens food security and the survival of the population ; bananas are a cash crop for example (economically crucial)
22
Q
Tuberculosis
A
Bacterial disease of humans, cows, pigs, badgers and deer caused by M.bovis - damages and destroys lung tissue and suppresses the immune system so body is more vulnerable to other diseases ; global rise of HIV/AIDS has had a big impact on the number of people suffering from TB because people who have AIDS are more likely to develop TB infections - TB is curable (antibiotics) and preventable (vaccination + living standards)
23
Q
HIV and TB link
A
HIV weakens immune system - increasing the risk of TB
24
Q
How to deal with TB affecting animals?
A
Very difficult to prevent them becoming re-infected from wildlife ; unsure how to control wildlife infection
Could cull the wildlife source (TB has been cut rapidly in cattle) - this must be done thoroughly or could lead to greater disease spread as animals are dispersed
Culling is not ethical and vaccination is better - however this is not easy and may not control spread of disease
25
Bacterial meningitis
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Bacterial infection (streptococcus pneumoniae) of the meninges of the brain (protective membranes in the surface of the brain) which can spread into the rest of the body causing septicaemia (blood poisoning) and rapid death
Mainly affects young children and teenagers with symptoms including red/purple rash that does not disappear when glass is pressed against it is a symptom of speicaemia
Antibiotics will cure the disease if delivered early and vaccines can protect against some forms
10% die
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26
HIV/AIDS
AIDS (acquired immunodeficiency syndrome) is caused by Human immunodeficiency virus which targets T helper cells in immune system - gradually destroys immune system so affected people are open to other infections like TB and pneumonia. Can also affect non%human primates - is a retrovirus with RNA genetic material
Contains reverse transcriptase - enzyme which transcribes RNA into single strand of DNA which interacts with the genetic material of the host cell ; virus is passed from one person to another via bodily fluids (unprotected sex/sharing needles/breast feeding)
No vaccine or no cure but anti retroviral drugs slow the profess of disease and give years of healthy life
Girls and women at high risk of AIDS - prominent in areas which practise FGM (female genitalia mutation) - same equipment is used many times it can spread infection - more vulnerable to the disease during intercourse if undergone FGM- SUB SAHARAN AFFICA IS THE WORST WITH 70% OF INFECTED GLOBALLY LIVING THERE ; SOCIAL AND ECONOMIC CONSEQUENCES
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Influenza
Viral infection of the ciliates epithelial cells in the gas exchange system - kills them, leaving the airways open to secondary infection - can be fatal for young children/elderly with chronic diseases… many of these deaths are from secondary bacterial infections like Pneumonia
Affects mammals and birds
3 strains with A being the most virulent (harmful)
Flu viruses mutate regularly - but these are quite small so immunity is left over if it is caught again BUT sometimes there is a major antigen changes causing a flu epidemic as no antibodies are available - vulnerable groups are continually given a flu vaccine to protect against the changing strains… no cure
28
Malaria
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Caused by the Protista plasmodia and spread by bites of infected mosquitoes (the vector) - plasmodium had a complex life cycle with two hosts (mosquitoes and people) ; they reproduce inside the female mosquito and she needs to take 2 blood meals to provide her with the protein before she lays her eggs - this is when Plasmodium is passed on to people and it invades red blood cells, liver and the brain
Disease recurs (continues periodically) making people vulnerable to other infections
No vaccine against malaria
Preventative measures can be effective - key is to control the vector ; anopheles mosquitoes can be destroyed by insecticides and by removing the standing water where they breed ; mosquito nets and door screens + long sleeved clothing can prevent them from biting people and spreading disease
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Ring worm
Fungal disease affecting mammals - differ fungi infect different species ; causes grey-white chest circular areas if skin ; anti fungal creams may be a cure and they are not damaging
30
Athlete’s foot
Human fungal disease - a form of human ring worm that browns on and digests the warm , moist skin between the toes causing cracking and scaling - anti fungal creams are an effective cure
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Two main types of transmission?
Direct and indirect transmission
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Direct transmission
Pathogen transferred directly from one individual to the other
Direct contact
Inoculation
Ingestion
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Examples of direct contact
Kissing or any contact with bodily fluids of another person (bacterial meningitis/STIs)
Direct skin to skin - ring worm (thus athletes foot)
Microorganism from faeces transmitted on the hands - diarrhoeal diseases
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Inoculation
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Break in the skin - during sex (HIV/AIDS)
Animal bite (rabies)
Puncture wound (septicaemia)
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Ingestion
Taking in contaminated food or drink or transferring pathogens to the mouth from the hands
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Indirect transmission?
From one individual to the next indirectly
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Fomites
Inanimate objects such as bedding, socks or cosmetics can transfer pathogens (athletes foot, staphylococcus infections)
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Inhalation
Droplet infection - minute droplets of saliva and mucus are expelled from your mouth as you talk/cough/sneeze - if these droplets contain pathogens, when healthy individuals breathe the droplets in they may become infected (influenza/tuberculosis)
39
Vectors
Vector transmits communicable pathogens from one hones to another - not always animals (mosquitoes with malaria)
Water can also act as a vector of disease (diarrhoea diseases)
40
Transmission between animals and humans?
Bird flu strain can be passed from sheep to people - minimise close contact with animals and wash hands thoroughly can reduce infection rates ; people can also act as vectors of some animal diseases with fatal results (foot and mouth disease)
41
What can reduce the spread of communicable diseases?
Regular hand washing - most effective way
Improvements in living and working conditions (reducing overcrowding and ensuring good nutrition)
Disposal of both bodily and household waste effectively
42
Factors affecting the transmission of communicable diseases in animals?
Overcrowding living and working conditions
Poor nutrition
Compromised immune system (HIV/AIDS or needing immunosuppressant drugs after transplant surgery)
Poor disposal of waste (breeding sites for vectors)
Climate change - tropical diseases spread over wider area
Culture and infrastructure - traditional medical practises can increase transmission
Socioeconomic factors - lack of trained health workers and insufficient public warning when there is an outbreak of disease
43
Transmission of pathogens between plants
Can be direct or indirect - direct involved direct contact if a healthy plant with any diseased plant : ring rot, TMV, black Sigatoka and the potato blight
44
Indirect transmission - soil contamination
Infected plants often leave pathogens or reproductive spores from fungi/Protista in the soil ; this can infect the next crop. Examples include black Sigatoka spores/ring rot bacteria, TMV or spores of P.Infestans
Some pathogens can survive the composting process so the infection cycle can be completed when contaminated compost is used
45
Indirect transmission vectors
Wind - viral/fungal/bacterial spores may be carried on the wind ; P.Infestans form spores which are carried by the wind to other potato crops/tomato plants
Water - spores swim in the surface film of water on leaves/raindrop splashes carry pathogens and spores - P.Infestans swims over films of water on the leaves
Animals - insects and birds carry pathogens and spores from one plant to another as they feed ; insects such as aphids inoculate pathogens directly into plant tissues
Humans - pathogens and spores are transmitted by hands, clothing, fomites, farming practises and transporting crops around the world ; TMV survives for years on crops and ring rot survives on farm machinery etc
46
Factors affecting transmission of communicable diseases in plants
Planting varieties of crops that are susceptible to disease
Overcrowding increases likelihood of direct contact
Poor mineral nutrition reduces resistance of plants
Damp/warm conditions increase survival and spread of spores
Climate change - increased rainfall and wind promote the spread of diseases ; changing conditions allow animal vectors to spread to new areas and drier conditions reduces the spread of disease
47
How to prevent spread of communicable diseases?
Leave room between plants to minimise the spread if pathogens
Clear fields as thou funky as possible - remove all traces of plants from the soil at harvesting
Rotate crops (spores/bacteria will eventually die if no access to host plant)
Strict hygiene - washing hands/washing boots and sterilising storage sack/machines
Control insect vectors
48
Examples of barrier defences on plants?
Waxy cuticle, bark on tress and cellulose cell walls - act as barriers to prevent pathogens getting in
Plants do not heal diseased tissue - they seal it off and sacrifice if because they are continually growing meristems which can replace the damaged areas
49
How to recognise an attack (plants)?
THEY ARE NOT PASSIVE
Receptors in cells respond to molecules from pathogens or to chemicals produced when cellulose wall is attacked - stimulates the release of signalling molecules that switch on genes in the nucleus. This triggers cellular responses which include defensive chemicals, sending alarm signals to unaffected cells to trigger defences and physically strengthening the cell walls
50
What happens when plants are attacked by pathogens?
They rapidly set up extra mechanical defences - produce high levels of polysaccharide callose with Beta 1,3 and beta 1,6 linkages between glucose monomers (DRAW THIS)
51
Roles of callose
Callose is synthesise and deposited between cell walls and membrane in cells next to infected cells next to infected cells - callose papillae act as barriers, preventing the pathogens entering the plant cells around the site of infection
Large amounts of callose continue to be deposited in cell walls after infill infection - lignin is also added, making the mechanical barrier to invasion thicker and stronger
Callose blocks sieve plates in the phloem to seal off the infected part and prevent the spread of pathogens
Callose is deposited in the plasmodesmata between infected cells and neighbours for seal them off from healthy cells and prevent pathogen spreading
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Chemical defences (plants)?
Many plants produce powerful chemicals that repel the insect vectors or kill invading pathogens - some of these are so powerful that we extract and use them to help control insects, fungi and bacteria
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Examples of plant defensive chemicals
Insect repellents - pine resin and citronella from lemon grass
Insecticides - pyrethrind which act as neurotoxins and caffeine which is toxic to insects and fungi
Antibacterial compounds - phenols (antiseptics made in many plants), defensins (plant proteins that disrupt bacterial and fungal cell membranes) and lysosomes (organelles containing hydrolytic enzymes which break down bacterial cell walls)
Antifungal compounds - phenols (antifungals too), caffeine (see above), saponins (interfere with fungal cell membranes), CHITINASES (ENZYMES WHICH BREAK DOWN CHITIN CELL WALL OF FUNGI)
ANTI-OOMYCETES - GLUCANASES - ENZYME THAT BREAKS DOWN GLUCANS WHICH IS A POLYMER FOUND IN FHE CELL WALL OF OOMYCETES LIKE P.INFESTANS
General toxins - form cyanide compounds which is toxic to most living things
54
How many lines of defence do mammals have against pathogens?
Primary non-specific defences which are always present/activated rapidly (defends against all pathogens in the same way) and also a specific immune response, which is specific to each pathogen but is slower to respond
55
What barriers does the body have to the entry of a pathogen?
The skin covers the body and prevents the entry of pathogens - it has a skin flora of healthy microorganisms that outcompete pathogens for space on the body surface. Also produces sebum which is an oily substance that inhibits the growth of pathogens
Many of the body tracts (including the airways) are lined by mucous membranes that secrete sticky mucus - this traps microorganisms and contains lysozymes which destroy bacterial and fungal cell walls… mucus also contains phagocytes which remove remaining pathogens
Lysozymes in tears and urine and the acid in the stomach also help to prevent pathogens getting into our bodies
56
Explosive reflexes?
Coughs and sneezes eject pathogen-laden mucus from the gas exchange system, while vomiting and diarrhoea expel the contents of the gut along with any infective pathogens
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What happens when you cut yours,Ed and are exposed to pathogens?
Skin is breached and blood clots rapidly to seal the wound - platelets + collagen in skin or the walls of damaged blood vessels leads to secretion of substances including
Thromboplastin - enzyme that triggers a cascade of reactions forming a blood clot
Serotonin - makes the smooth muscle in the walls of the vessels contract so they narrow and reduce blood flow to the area
Clot dries out forming a hard scab which keeps pathogens out - FIRST STEP OF WOUND REPAIR
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Next step of wound repair?
Epidermal cells grow to seal the wound permanently while damaged blood vessels also regrow
Collagen fibres are deposited to give the new tissue strength -p
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Blood clotting cascade flowchart
Theomboplastin catalyses the conversion of prothrombin (+Ca2+ ions) to thrombin ; thrombin then catalyses fibrinogen into fibrin which forms a clot
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What is an inflammatory response?
A localised response to pathogens resulting in inflammation at the site of a wound - inflammation is characterised by pain, heat, redness and swelling of tissue
Inflammation is the biological response of vascular tissue to pathogens and damaged cells
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What happens in an inflammatory response?
Mast cells are activated in damaged tissue and release chemicals called histamines and cytokines
Histamines make the blood vessels dilate - causing localised heat and redness, raised temperature prevents pathogens reproducing
Histamines make the vessels more leaky so plasma is forced out and this creates tissue fluid - causing oedema and pain (at lymph nodes)
Cytokines attract phagocytes to the site and they dispose of pathogens through phagocytosis
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What is phagocytosis?
Phagocytes recognise non-self cells, engulf them and digest them within a vesicle called a phagolysosome
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What happens if pathogens get into the body?
Non-specific defences must adapt to prevent them growing or destroy them
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Non-specific defences (once pathogens enter)
Fevers - normal body temperature of around 37 degrees is maintained by the hypothalamus and when a pathogen invades your body, cytokines stimulate your hypothalamus to reset the thermostat and your temperature goes up
This inhibits pathogen reproduction (most reproduces less than 37 degrees)
Specific immune system also works faster at higher temperatures
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Two main types of phagocytes?
Neutrophils and macrophages
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What happens at the site of an infection?
Phagocytes build up and attack pathogens - you can see pus in a spot/wound ; this consists of dead neutrophils and pathogens
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Stages of phagocytosis
1) Pathogens produce chemicals that attract phagocytes
2) Phagocytes recognise non-human proteins on the pathogen. This is a response not a specific type of pathogen but simply a self that is non-self
3) Pahgocytes engulf the pathogen and enclose if in a vacuole called a phagosome
4) This phagosome combines with a lysosome to form a phagolysosome
5) Hydrolytic enzymes digest and destroy the pathogen
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Why is it different for macrophages?
When a macrophage has digested a pathogen - it combines antigens from that pathogen with special glycoproteins in the cytoplasm called the major histocompatibility complex ; this moves the antigens to the macrophage’s surface membrane and it now becomes an Antigen Presenting Cell. These APCs nos stimulate other cells involved in the specific immune system response
69
When counting blood cells?
Blood smear - spread thinly
Often stained to show the nuclei of lymphocytes, making them easier to identify (multi lobed nuclei for neutrophils and a simple round one for macrophages)
Specific = more lymphocytes
Non-specific = less lymphocytes (more phagocytes)
70
Cytokines?
Phagocytes have engulfed a pathogen produce chemicals called cytokines - they act as cell-signalling molecules, informing other phagocytes that the body is under attack and stimulating them to move to the site of inflammation. They also increase body temp and stimulate the specific immune system
71
Opsonins
Chemicals that bind to pathogens and tag them so they can be more easily recognised by phagocytes - they have receptors on their cell membranes that bind to common opsonins and the phagocytes then engulfs the pathogen. A number of different opsonins but antibodies such as immunoglobulin IgG and IgM have the strongest effect
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Antigens?
All cells have molecules called antigens on their surface - body recognised between self antigens and non-self antigens ; they trigger an immune response which involves the production of polypeptides called antibodies
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Specific immune system comparison?
Also known as active/acquired immunity
Slower than non-specific responses ; it can take up to 14 days to respond effectively to a pathogen invasion - but the immune memory cells mean it reacts very quickly to a second invasion by the same pathogen
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What are antibodies?
Y-shaped glycoproteins called immunoglobulins which bind to a specific antigen on the pathogen/toxin that has triggered the immune response ; SPECIFIC antibody for each antigen
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Antibodies composition?
Made up of two identical long polypeptide chains called the heavy chains and two much shorter identical chains called the light chains ; they are held together by disulphide bridges and there are also disulphide bridges within the polypeptide chains holding them in shape
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DRAW AN ANTIBODY
Drawn (pg 320)
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How do antibodies bind to antigens?
With a protein-based “lock and key” mechanism - binding site is an area of 110 amino acids on the heavy and light chains, known as the variable region (different on each antibody). This gives it its specificity. The rest of the antibody molecule is always the same - constant region
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Antibody + antigen
Antigen-antibody complex
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Hinge region on antibody?
Provides the molecule with flexibility, allowing it to bind to two separate antigens - one at each of its antigen binding sites
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How do antibodies defend the body?
1) Antibody acts as an opsonin so the complex is easily engulfed and digested by phagocytes
2) Most pathogens can no longer effectively invade the host cells once they are part of an antigen-antibody complex
3) Antibodies act as Agglutinins causing pathogens carrying antigen-antibody complexes to clump together - thus prevents them from spreading through the body and makes it easier for phagocytes to engulf a number of pathogens at once
4) Antibodies also act as anti-toxins, binding to the toxins produced by pathogens and making them harmless
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Where do B lymphocytes mature?
In the bone marrow
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Where do T lymphocytes mature?
In the thymus gland
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Specific immune system is based on
White blood cells called lymphocytes
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Main types of T lymphocytes
T helper cells
T killer cells
T memory cells
T regulator cells
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T helper cells
They have CD4 receptors which bind to the surface antigens on APCs - they produce interleukins (cytokines) ; they stimulate the activity of B cells which increase antibody production, stimulates production of other T cells and attracts macrophages to ingest pathogens with antigen-antibody complexes
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T killer cells
Destroy pathogens carrying the antigen - produce a chemical called Perforin which kills the pathogen by making holes in the cell membrane so it is freely permeable
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T memory cells
Live for a long time and are part of the immunological memory ; if they meet an antigen a second time, they divide rapidly to form a huge number of clones of T killer cells (clonal expansion is rapid) that destroys the pathogen
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T regulator cells
They suppress the immune system and control/regulate it - stop the immune response once a pathogen has been eliminated and does not set your an autoimmune response (against healthy tissue) - interleukins are important in this
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B lymphocytes
Plasma cells
B effector cells
B memory cells
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Plasma cells
Produce antibodies to a particular antigen and release them into the circulation ; only lives for a few days but produces around 2000 antibodies per second while active
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B effector cells
Divide to form plasma cell clones
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B memory cells
Live for a very long time and provide immunological memory - they are programmed to remember a specific antigen and enable the body to make a very rapid response when a pathogen carrying that antigen is encountered again
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Cell-mediated immunity
T lymphocytes respond to the cells of an organism that have been changed in some way (by a virus infection/by mutation/antigen processing) and to cells from transplanted tissue ; particularly important against viruses and early cancers
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Process of cell-mediated immunity
Macrophages engulf and digest pathogens in phagocytosis - they process the antigens from the surface of the pathogen to form APCs
The receptors on some of the T helper cells fit the antigens - these T helper cells become activated and produce interleukins ; stimulate more T cells to divide rapidly by mitosis. Form clones of identical activated T helper cells that all carry the right antigen to bind to a particular pathogen
Cloned T cells may
- develop into T memory cells which give a rapid response if pathogen invades the body
- produce interleukins that stimulate phagocytosis
- produce interleukins that stimulate B cells to divide
- stimulate the development of a clone of T killer cells that are specific to the presented antigen and then destroy the infected cells
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Hum oral immunity?
Body responds to antigens found outside the cells - bacteria and fungi and to APCS ; they produce antibodies that are soluble in the blood and tissue fluid and are not attached to cells
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Humoral immunity B lymphocytes
When a pathogen enters the body carrying specific antigens, a B cell with the complementary antibodies will bind to the antigens on the pathogen or to the free antigens - the B cell engulfs and processes the antigens to become an APC
Activated T helper cells bind to the B cell APC (CLONAL SELECTION)
Interleukins produced by the activated T helper cells activate B cells
The activated B cell divides by mitosis to give clones of plasma and B memory cells - CLONAL EXPANSION
Cloned plasma cells produce antibodies that fit the antigens on the surface of the pathogen, bind and act as opsonins/Agglutinins. THIS IS PRIMARY IMMUNE RESPONSE AND CAN TAKE DAYS/WEEKS TO BE EFFECTIVE - SYMPTOMS ARE THE RESULT OF THE WAY OUR BODY REACTS WHEN THE PATHOGENS ARE DIVIDING FREELY
B memory cells divide rapidly to form plasma cell clones if infected by same pathogen - produce right antibody to wipe out the pathogen before symptoms of disease (secondary immune response) - memory cells always circulate in blood and tissue fluid
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Autoimmune disease
When immune system stops recognising self cells and start to attack healthy body tissue - appears to be a genetic tendency in some families, sometimes the immune system responds abnormally to a mild pathogen
They can cause chronic inflammation or complete breakdown of healthy tissue - immunosuppressant drugs, which prevent the immune system working, may be used as treatment but they deprive the body of its natural defences against communicable diseases (vulnerable)
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Draw graph on primary and secondary immune response
PG 323
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Type 1 diabetes
Affects the insulin secreting cells of the pancreas
| Treatment is insulin injections, pancreas transplants and immunosuppressant drugs
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Rheumatoid arthritis
Joints are affected (hands, wrists, ankles and feet)
| Treatment - no cure but anti inflammatory drugs, steroids, pain relief and immunosuppressants can be used)
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Lupus
Affects the skin and joints (causing fatigue)/can attack any organ including kidney, liver and brain
No cure but anti-inflammatory drugs, steroids and immunosuppressants can be used
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Natural active immunity
When you are exposed to a pathogen for the first time - antibodies are formed and also T and B memory cells are produced to build immunological memory (before it can cause symptoms) - natural active immunity as the body has itself acted to produce antibodies/memory cells
IMMUNITY HAS OCCURRED NATURALLY IN THE BODY
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Natural passive immunity
Immune system of a new-born baby is not mature and it can’t make antibodies so some antibodies cross the placenta from the mother to her foetus while the baby is in the uterus
First milk a mammalian mother makes is called COLOSTRUM - very high in antibodies - infant gut allows these glycoproteins to pass into bloodstream so within a few days the Brest fed baby will have the same level of antibody protection as the mother. Lasts until able to make its own antibodies - these antibodies are relevant to pathogens in its environment where the mother acquired them
This is natural passive as it is acquired by immunity gained from someone else
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Artficial immunity
Immunity to diseases without any contact with live pathogens - not internally created
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Artificial passive immunity
Antibodies are formed in one individual (animal), extracted and then injected into the bloodstream of another individual - this gives temporary immunity and doesn’t last long ; series of injections
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Artificial active immunity
Immune system if the body is stimulated to make its own antibodies to a safe form of an antigen (a vaccine) which is injected into the bloodstream
Pathogen is made safe so antigen have no risk of infection - vaccines may contain
Inactivated bacteria/viruses (whooping cough)
Attenuated strains of live bacteria (BCG/rubella)
Toxin molecules that have been detoxified (tetanus)
Isolated antigens from the pathogen (influenza)
Genetically engineered antigens (hep B)
Small amounts of vaccine are injected into the blood
Primary immune response is triggered and body produced antibodies and memory cells
Secondary immune response is triggered if contact the second time - destroy pathogen rapidly before symptoms are suffered
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Length of vaccines?
Year/few years or a lifetime - boosters may be needed to increase the time you are immune to a disease
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Vaccines and epidemics?
They can be used to help prevent epidemics (communicable diseases spread rapidly to a lot of people on a local/national level). Pandemic is when same disease spreads rapidly across a number of countries/continents
MASS VACCINATION can prevent spread of the pathogen into wider population - often have to be changed to remain effective (mutating)
When a significant number of people in the population have been vaccinated, this gives protection for those who don’t have immunity - THIS IS HERD IMMUNITY SO MINIMAL OPPORTUNITY FOR OUTBREAK TO OCCUR
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Some communicable diseases that cause problems at a global level?
Cannot be prevented by vaccination
Malaria - Protista that cause malaria are very evasive and spends time inside erythrocytes so it is protected from the immune system by self antigens
HIV - enters macrophages and T helper cells so it has disabled the immune system itself
Affects millions globally every year
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Sources of medicines
Penicillin was the first - came from a mould (Fleming) but this process has to be adapted to suit industrial processes to make this new drug
Medicines we use today come from a wide range of sources - computers are used to search through many chemicals, to isolate any with a potentially useful action against a specific pathogen etc
Analysis of genes has allowed novel therapies against cancer - attacks vulnerabilities ; many of the drugs still used are based on bio active compounds discovered in plants/microorganisms
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Penicillin
Source is from mould growing on melons
| Action - antibiotic against many bacterial diseases
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Aspirin
Source - compounds from sallow bark (willow)
| Action - painkiller and anti-inflammatory
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Prialt
Source - derived from venom of a cone snail
| Action % pain-killing drug 1000 times more effective than morphine
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Vancomycin
Source - derived from a soil fungus
| Action - one of our most powerful antibiotics
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Biodiversity and medicines?
Rapidly being lost around the world including the destruction of rain forests and loss of coral reefs and loss of habitats for natural ecosystems in countries all around the world - partially due to human activities ; we should not destroy plant, animal or microorganism which could give us the key to a life saving drug
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Pharmacogenetics (pharmacogenomics)
Personalised medicine - a combination of drugs that work with your individual combination of genetics and disease ; human genome can be analysed rapidly and cheaply giving us a better understanding of the genetic bases behind diseases ; interweaving this with knowledge of drug actions is pharmacogenomics
Treat people with the mutation of the HER2 gene (breast cancer). Decreases deaths by 50% ; clinicians will look at the genome of patient and of the pathogen before deciding how to treat them
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Synthetic biology
Using genetic engineering, we can develop populations of bacteria to produce much needed drugs that would be too rare or expensive ; uses bacteria as biological factories - divide rapidly through binary fission
Mammals have been genetically modified to produce more proteins in their milk
Nanotechnology is another strand of synthetic biology where tiny particles are used to deliver drugs to specific sites within cells of pathogens/tumours
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How do antibiotics work?
They interfere with the metabolism of bacteria without affecting human cells - this is called selective toxicity ; range if antibiotics used against these many different types of bacteria
Often used for minor infections where immune system of the patient would deal with the infection with no serious difficulty
THEY ARE BECOMING LESS EFFECTIVE DUR TO RESISTANCE - STARTED WITH PENICILLIN AND NOW THERE ARE SOME THAT ARE FULLY RESISTANT
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Development of antibiotic resistance?
Antibiotic works because bacterium has a binding site for the drug and a metabolic pathway that is affected by the drug ; if a random mutation during binary fission causes a bacterium that is nit affected by an antibiotic, it survives (of the fittest) and reproduces, passing on this advantageous antibiotic resistance mutation to daughter cells
Once a mutation occurs it does not take long to grow a big population of antibiotic-resistant bacteria
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Future of antibiotic resistance
In a few decades - all bacteria will be antibiotic resistant and we will not have the resources to continue making new ones
Many routine exposures (such as antibiotics to animal feed prophylactically ) accelerates the rate of natural selection of antibiotic-resistant strains ; in U.K. it is illegal to give animals routine antibiotics
Over-subscription is the prime cause of the rise in antibiotic resistance
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Flowchart of antibiotic resistance
Chance mutation in a bacterium produces a gene for antibiotic-resistance
Antibiotic A applies a selection pressure - there is strong natural selection for bacteria with a gene for antibiotic resistance ; leading to a population with a lot of antibiotic resistance
Continued selection pressure means almost all bacteria in the population will be antibiotic resistant
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Where is antibiotic resistance a big problem?
In hospitals and care homes for older people where they are often needed and used ; MRSA and C.Difficile are high profile examples of antibiotic-resignation bacteria
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MRSA
Methicillin resistant
Can cause boils and fatal septicaemia
Was treated effectively with methicillin but mutation has produced resistant strains
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C.difficile
Produces toxins that damage the lining of the intestines, leading to diarrhoea/bleeding
When commonly used antibiotics kill a lot of the helpful flora, it reproduces and becomes dominant, taking hold rapidly
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How can antibiotic resistance be reduced?
Minimise the use of antibiotics - ensure every course is completed to reduce the risk of resistant individuals surviving and developing into a resistant strain population
Good hygiene in general - major impact on all spreads of infections
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How is the problem being solved of antibiotic resistance?
Fear that we may return to the days when bacterial infections killed thousands of people each year in the U.K. alone
Developing new antibiotics using computer modelling and soil microorganisms/Crocodile blood etc
Bacterial resistance faster than new antibiotics found
Incentives put forward for anyone who can come up with a cost-effective, accurate way to reduce bacterial infections so that doctors can use the right antibiotics at the right time and only when they are needed
