communicable disease Flashcards
1
Q
what is disease
A
A disease is an illness or disorder of the body or mind that leads to poor health
Each disease is associated with a set of signs and symptoms
Communicable/infectious diseases are caused by pathogens and are transmissible (can be spread between individuals within a population)
Both plants and animals can be affected by pathogens
2
Q
infectious and non infectious diseases
A
infectious disease- these are diseases cause by organisms know as pathogens. they are sometimes called communicable diseases as they are passed from infected to uninfected people (transmittable) some also affect animals and are passed from animal to humans
examples: cholera, malaria, HIV/AIDs
non-infectious disease- these are long term degenerative diseases that are not caused by pathogens. examples include diseases of the gas exchange and cardiovascular systems, inherited or genetic diseases, deficiency diseases caused by malnutrition, and mental diseases
examples: lung cancer, cystic fibrosis, sickle cell anaemia
3
Q
types of pathogens
A
Bacteria
Viruses
Fungi
Protoctists
To control disease, it is very important to know what pathogen is causing it
4
Q
bacteria
A
Bacteria are a diverse range of prokaryotic organisms
Some bacteria are non-pathogenic (they do not cause any disease or damage) while others are pathogenic
Pathogenic bacteria do not always infect the hosts of cells, they can remain within body cavities or spaces
5
Q
tuberculosis
A
M. tuberculosis causes tuberculosis (TB) in humans
The bacteria infect the lungs, causing a chronic cough and bloody mucus
It is a disease often associated with poor hygiene and sanitation
M. bovine in cows can also transmit to humans to cause TB
6
Q
bacterial meningitis
A
N. meningitidis causes bacterial meningitis in humans
Very few bacteria can cross the barrier created by the meninges (the tissue that surrounds the brain and spinal cord) however N. meningitidis crosses this barrier to cause acute inflammation
Inflammation of the meninges causes symptoms such as fever, headache, neck stiffness and a characteristic rash
7
Q
ring rot
A
Ring rot diseases in potato plants are caused by bacterial pathogens
The bacteria infect the vascular tissue and prevent the transport of water, causing the plant to wilt and die
The infection spreads into the potato tubers where the vascular tissue is arranged in a ring, producing the characteristic black ring of rot
8
Q
viruses
A
Viruses do not have a cellular structure
This means they can’t respire, produce ATP, replicate genetic material or synthesise protein
They infect host cells and hijack their machinery to replicate their own genetic material and proteins
9
Q
tobacco mosaic virus
A
The first virus ever discovered was the Tobacco Mosaic Virus (TMV)
TMV infects several plant species
It causes a distinct yellowing of the leaves which produces a mosaic pattern
10
Q
influenza viruses
A
Three different influenza viruses infect humans to cause the flu
Influenza A, influenza B and influenza C infect the cells that line the airways
They cause a high temperature, body aches and fatigue
Influenza A is the virus that causes the most cases of flu globally
It has a capsid that surrounds 8 single-stranded molecules of RNA
11
Q
HIV
A
The human immunodeficiency virus (HIV) infects specific cells of the immune system
It is an enveloped retrovirus
The viral enzyme reverse transcriptase produces single-stranded DNA from its viral RNA
DNA polymerase synthesises double-stranded DNA from this single-stranded DNA
The double-stranded DNA is inserted into the host DNA and can remain inactive for many years
Once activated the DNA provirus is used to synthesise new viruses
12
Q
protoctista (protists)
A
Protists are unicellular eukaryotes
13
Q
malaria
A
Plasmodium falciparum is a protist that causes severe forms of malaria in humans
The parasite is spread by mosquitoes
Infected individuals experience fever, chills and fatigue
14
Q
potato blight
A
P. infestans causes the infamous potato blight
The pathogen is unusual as it has some fungal characteristics
It is transmitted via spores
The first signs of potato blight are small, dark brown marks on the leaves which quickly increase in size and number
The protist destroys potato and tomato crops leaving them completely inedible
15
Q
fungi
A
Fungi have a similar structure to plants
Their eukaryotic cells have cell walls and large central vacuoles
However, instead of being made of separate cells, their bodies consist of filaments known as hyphae
These hyphae form a network and spread throughout a host/soil
Fungal diseases are much more common in plants than animals
16
Q
cattle ringworm and athletes foot
A
Cattle ringworm and athletes foot are fungal diseases that exist on the surface of the skin
17
Q
black sigatoka
A
Fungal diseases in plants tend to be much more serious and can threaten entire crops
Black Sigatoka is a fungal disease in bananas
It spreads through the leaves of the plant, reducing its ability to photosynthesise
The lack of photosynthesis causes parts of the leaf to die; producing black streaks
Eventually, the whole leaf dies
18
Q
disease transmission
A
In order for a population of pathogens to survive, they must be able to successfully transfer from host to host
If pathogens are unable to find new hosts then they will go extinct
Disease transmission is defined as the transfer of pathogens from an infected host to an uninfected host
Transmission can be very risky for pathogens
During the infective stages, pathogens produce a large number of individuals to increase the likelihood that some will find a new host and survive
There are two types of disease transmission:
Direct - from one host to another host
Indirect - a second organism (vector) that is unaffected by the pathogen transfers it to a new host
19
Q
direct transmission
A
The direct transmission of a pathogen can involve physical contact between individuals
If the leaves of plants infected with Tobacco Mosaic Virus (TMV) touch the leaves of another uninfected plant, particles of the virus are transmitted
Sometimes individuals being within close proximity to each other is sufficient for direct transmission
The influenza viruses are spread in the air via tiny droplets of water. An infected individual breathes out droplets containing the virus and they are breathed in by an uninfected individual
Spores can also be involved in the direct transmission of pathogens
Spores are very small reproductive structures that are released into the environment. They are dispersed via wind or water
Once they reach a food source (host) they begin growing
Depending on the organism, spores can be produced via mitosis or meiosis so they can be haploid or diploid
P. infestans which causes potato blight produces specialised spores called sporangia. These structures are adapted for wind dispersal
20
Q
transmission of HIV/AIDS
A
Human Immunodeficiency Virus is a retrovirus
The HIV virus is not transmitted by a vector (unlike in malaria)
The virus is unable to survive outside of the human body
HIV is spread by intimate human contact and can only be transmitted by direct exchange of body fluids
This means HIV can be transmitted in the following ways:
-sexual intercourse
-blood donation
-sharing of needles used by intravenous drug users
-from mother to child across the placenta
mixing of blood between mother and child during birth
-from mother to child through breast milk
21
Q
transmission of tuberculosis
A
When infected people with the active form of the disease cough or sneeze, the Mycobacterium tuberculosis bacteria enter the air in tiny droplets of liquid
TB is transmitted when uninfected people then inhale these droplets
TB, therefore, spreads more quickly among people living in overcrowded conditions
The form of TB caused by Mycobacterium bovis occurs in cattle but is spread to humans through contaminated meat and unpasteurised milk
Very few people in developed countries now acquire TB in this way, although meat and milk can still be a source of infection in some developing countries
22
Q
indirect transmission
A
Vectors are involved in the indirect transmission of pathogens
A vector is any organism that transfers a pathogen from an infected individual to an uninfected individual
The vector themselves usually aren’t harmed by the pathogen
A lot of disease vectors tend to be insects
Insects are ideal vectors as they reproduce in large numbers which increases the likelihood of pathogen transmission
23
Q
transmission of malaria
A
Malaria is caused by one of four species of the protoctist Plasmodium
These protoctists are transmitted to humans by an insect vector:
Female Anopheles mosquitoes feed on human blood to obtain the protein they need to develop their eggs
If the person they bite is infected with Plasmodium, the mosquito will take up some of the pathogen with the blood meal
When feeding on the next human, Plasmodium pass from the mosquito to the new human’s blood
Malaria may also be transmitted during blood transfusion and when unsterile needles are re-used
Plasmodium can also pass from mother to child across the placenta
24
Q
factors that affect disease transmission
A
The transmission of disease ultimately depends on:
The presence of the pathogens
If the pathogen is not present in the population then it cannot spread
The presence of susceptible individuals
A high number of immune or resistant individuals in a population will reduce the likelihood of transmission
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resistance to disease
Animals and plants can be resistant to some diseases
Individuals who are resistant have mechanisms that prevent the infection or spread of pathogens within their body. They are not susceptible to disease.
These mechanisms are coded for by their genes
Individuals who are heterozygous for the sickle cell allele have resistance to malaria
Some humans are even resistant to HIV
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resistance vs immunity
When resistant individuals are exposed to the pathogen for the first time they do not develop the disease and suffer no symptoms
An immune individual has been previously infected with the pathogen, suffered symptoms of the disease and recovered.
They are highly unlikely to develop symptoms of the disease when exposed to the pathogen again
The proportion of resistant or immune individuals in a population influences the potential for transmission (as they are not susceptible to disease)
The higher the proportion, the lower the probability of transmission
Different types of disease transmission are affected by different factors
Human pathogens are affected by specific factors dictated by human behaviour and population size
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factors affecting direct transmission
Pathogens that spread through direct contact or by droplet infection need potential hosts to be within close proximity to each other
Places or areas with high population densities are more likely to have high infection rates
E.g. cities and schools
Tuberculosis (TB) transmission is very high in places where many people have to sleep in confined quarters
E.g. poor housing and homeless shelters
Farmers who use monocultures to maximise yield and profit can experience large disease outbreaks
Farmers grow a large number of crop plants in a small area
As the crops grow the leaves of different plants touch each other, making the transmission of pathogens such as tobacco mosaic virus (TMV) very easy
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factors affecting indirect transmission
The indirect transmission of a pathogen can be affected by the biology of the vectors involved
Common disease vectors include mosquitoes and aphids
The population of vectors (usually insects) is influenced by weather and climate
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factors affecting the distribution of malaria
Malaria is caused by one of four species of the protoctist Plasmodium but these protoctists are transmitted to humans by an insect vector (female Anopheles mosquitoes)
The Anopheles mosquitoes favour habitats that have high rainfall, high temperatures and high humidity
This means malaria can occur where these mosquitoes are present and, as a result, is found throughout the tropics and sub-tropics (about 80% of cases are in Africa)
The Anopheles mosquitoes found in Africa also have longer lifespans and prefer biting humans than animals
30
research regarding malaria
In the 1950s, the World Health Organisation (WHO) coordinated a worldwide eradication programme.
Whilst malaria was eradicated from some countries, the programme was mainly unsuccessful because:
Plasmodium became resistant to the drugs being used to try and control it
Anopheles mosquitoes became resistant to DDT and other insecticides being used against them
There is evidence that there are an increasing number of malaria epidemics due to climatic and environmental changes that favour the spread of the Anopheles mosquitoes
31
social factor of the spread of malaria
A social factor that has caused the number of cases of malaria in Africa, in particular, to increase in recent years is the increased migration of people due to war (when migration happens due to war the parasite can be transferred from areas that have the infection to new regions, and, if the Anopheles mosquito is breeding in the new region, then the mosquito vector will transfer the disease from one human to the next)
32
The degree or level of poverty in an area effecting transmission of disease in humans
Water-borne disease like typhoid, cholera and polio spread when human faecal matter enters and contaminates drinking water
Those below the poverty line usually live in areas with crowded housing with no sewage systems, sanitation facilities or water treatment facilities. In addition, many people in these areas have limited access to hygiene products
In the last 200 years, humans have spread across the globe, bringing their diseases and pathogens with them
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the level of human movement and migrations effect on transmission of human disease
The level of human movement and migration that currently exists means that populations are more connected than ever
In the past, the ocean and bodies of water would have acted as natural geographic barriers to prevent the spread of pathogens
The first flu pandemic in 1918 took one year to spread around the globe. The flu pandemic in 2009 only took 3 months to reach West Africa from North America
An individual can become infected in one country (where the disease exists) and get a flight to another country thousands of miles away. They may not show any symptoms until they have already arrived in the new country
The historical danger of human migration is well known
When colonisers arrived in the Americas they brought many European diseases with them, such as smallpox
The Native Americans had no immunity or resistance as they had never been exposed to these pathogens before (they were a fully susceptible population)
The invasive pathogens rapidly spread through the population causing a large number of deaths
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the behaviour or cultural practices of humans on the spread of disease
The behaviour or cultural practices of humans can also affect the transmission rate of diseases
For example, in parts of Africa, it is a religious and cultural tradition to touch and kiss the dead. This was a major problem during Ebola outbreaks there and scientists had to work with the public to try and inform them that this tradition was increasing the spread of the virus
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endemic, epidemic, pandemic
Endemic - a disease that is always present in a population (even if very low numbers)
Epidemic - there is a large increase in the number of cases in a population (an outbreak)
Pandemic - an epidemic occurs on a large scale and crosses international boundaries
36
passive defences in plants
Passive defence mechanisms are always present
Some of these mechanisms are physical barriers that prevent pathogens from entering
Some are chemicals that reduce or prevent the growth of pathogens
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active defences in plants
Active defence mechanisms in plants are activated when pathogens invade
Hypersensitivity deprives pathogens of resources
The formation of physical barriers by callose plays a major role in limiting the spread of pathogens
Cell signalling plays an important role in coordinating the active defence mechanisms
38
passive defence mechanisms
Physical barriers make it harder for pathogens to gain entry into plants
Examples of physical barriers:
Waxy cuticle
The only way that viruses and bacteria can penetrate the waxy cuticle of a leaf is if there is a wound on the leaf surface or stem.
Wounds are commonly caused by grazing herbivores
Cellulose cell wall
Closed stomata
Bark
Casparian strip
Some fungi species can invade a plant all the way to the endodermis but they are unable to push past the Casparian strip
Chemical defences prevent pathogens from growing on the surface of the plant by creating acidic conditions
Examples of chemical defences:
Toxic compounds
E.g. Catechol
Sticky resin found in the bark
This traps the pathogens so they can't spread
Compounds that encourage the growth of competing microorganisms
Microorganisms such as yeast found on the leaf surface are completely harmless to plants. They are strong competitors against harmful pathogens
Enzyme inhibitors
E.g. Tannins
Receptor molecules
They detect the presence of pathogens and trigger other defence mechanisms
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active defence mechanisms
Unlike animal cells, plant cells have cell walls. This means that substances can not freely move around the entire plant as the immune cells do in some animals, making cell signalling vital for plant defence
The active defence mechanisms of a plant are activated once a pathogen has invaded
Hypersensitivity is the rapid death of tissue surrounding the infection site
Although quite an extreme response, it is very effective as it deprives the pathogens of host tissue, nutrients and energy
Plants also create physical barriers to reduce the spread of a pathogen
Reinforced cell walls are formed when fungi and bacteria invade
-The invasion of pathogens stimulates the release of compounds callose and lignin
-These molecules are deposited between the cell surface membrane and the cell wall
-Callose is a polysaccharide that forms a matrix shape. Antimicrobial compounds that kill pathogens (hydrogen peroxide and phenols) can be deposited in this shape
Narrowing of the plasmodesmata
-Callose helps to reduce the size of the channels that connect neighbouring plant cells
Ingrowths into the xylem vessels (tyloses)
-The cytoplasm of nearby cells grows into the xylem to create a wall made of callose
Blockage of the phloem
-The sieve pores are filled with callose which prevents phloem sap from being transported
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the importance of cell signalling in plant defences
Pathogens possess cellulase enzymes that digest the cellulose in plant cell walls
The molecules produced from this breakdown of cellulose act as signals to cell surface receptors
By stimulating these receptors they cause the release of defence chemicals called phytoalexins
Phytoalexins have several modes of action
-Disrupting pathogen metabolism
-Delaying pathogen reproduction
-Disrupting bacterial cell surface membranes
-Stimulating the release of chitinases (enzymes that break down the chitin cell walls in fungi)
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chemicals involves in cell signalling
Salicylic acid is another important signalling molecule involved in plant defence
It migrates through the plant to uninfected areas.
Once there it activates defence mechanisms that protect the plant against pathogens for a period of time
This long-term protection is called systemic acquired resistance
Ethylene is a signalling compound that allows plants to communicate
Plants under attack from pathogens secrete ethylene onto their leaves. The ethylene vaporises, stimulating other leaves on the same plant to react (as well as other plants)
42
non specific immune response
Physical: body tissues act as barriers, preventing the entry of pathogens
E.g. skin, mucous membrane of the alimentary canal
Cellular: cells detect and signal the presence of pathogens. Protective substances are secreted and the pathogens are ingested and digested
Chemical: secreted substances generate an inhospitable environment for the growth of pathogens. These substances can trap pathogens, cause them to burst, or prevent them from entering cells and reproducing
Commensal organisms: the harmless bacteria and fungi present on and in the body compete with pathogens for nutrients
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first line of defence
a human has three lines of defence
The first line of defence prevents the entry of pathogens and is comprised of the following:
-Skin
-Mucous membranes
-Expulsive reflexes
-Chemical secretions
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skin
Skin posses an outer layer of dry, dead, hardened cells filled with keratin
Keratin is a tough fibrous protein
This layer of cells acts as a physical barrier to pathogens
There are secretions of sebum that contain fatty acids which have antimicrobial properties
Evaporation of sweat from the skin leaves behind a salt residue
The lack of moisture, low pH and high salinity creates an inhospitable environment for the growth of microorganisms
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mucous membranes
Mucous membranes line the gut, airways and reproductive system
The mucous membrane consists of epithelial cells and mucus-secreting cells like goblet cells
Mucus contains lots of glycoproteins with long carbohydrate chains. These chains are what make mucus sticky
Viruses, bacteria, pollen and dust float about in the air that we breathe in
Mucus in the airways (trachea, bronchi and bronchioles) can trap these particles
The particles are then moved towards the back of the throat by cilia
Cilia are small hair-like structures on the surface of cells. Some ciliated epithelial cells have motile cilia that beat and move in a wave-like manner to move mucus along the airway
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exclusive reflexes
When a pathogen irritates the lining of an airway it can trigger an expulsive reflex; a cough or sneeze
Both a cough and sneeze result in a sudden expulsion of air. This expelled air contains secretions from the respiratory tract along with the foreign particles that have entered
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chemical secretions
Lysozymes are antimicrobial enzymes that breakdown the cell wall of bacteria
These special enzymes are found in body fluids such as blood, tears, sweat, and breast milk
Hydrochloric acid is produced by the cells that line the stomach
The acid creates a low pH inside the stomach which helps to kill any bacteria that has been ingested alongside food
The cells of the gut secrete mucus to prevent being damaged by hydrochloric acid
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commensalism microorganisms
On average roughly 1kg of a human's weight is made up of the bacteria on or inside their body
Candida albicans and E. coli are examples of bacteria commonly found on and in humans
These microorganisms grow on the skin, in the mouth and intestines however they do not cause disease
Their growth is limited by the defence mechanisms
Hosting these microorganisms can have a major benefit for humans
They compete with pathogenic microorganisms and prevent them from invading host tissue
Antibiotics often kill friendly gut bacteria which can allow for opportunistic pathogens to grow
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second line of defence
When a pathogen manages to evade the first line of defence then the second line of defence will respond
The second line of defence involves phagocytic cells and antimicrobial proteins responding to the invading pathogens
Second-line responses include:
-Blood clotting
-Inflammation
-Wound repair
-Phagocytosis
50
blood clotting
When the body is wounded it responds rapidly
A break in the mucous membranes or skin membranes causes the release of molecules that trigger a chemical cascade which results in blood clotting
Blood clotting prevents excess blood loss, the entry of pathogens and provides a barrier (scab) for wound healing to occur
The chemical cascade involves a large number of steps and several plasma proteins
A small initial stimulus is amplified to produce a large amount of fibrin so that the wound is quickly sealed
51
inflammation
The surrounding area of a wound can sometimes become swollen, warm and painful to touch; this is described as inflammation
Inflammation is a local response to infection and tissue damage. It occurs via chemical signalling molecules which cause the migration of phagocytes into the tissue and increased blood flow
Body cells called mast cells respond to tissue damage by secreting the cell signalling molecule, histamine
52
histamine and cytokines
Histamine stimulates the following responses:
-Vasodilation increases blood flow through capillaries
-"Leaky" capillaries allow fluid to enter the tissues and creating swelling
-A portion of the plasma proteins leave the blood
-Phagocytes leave the blood and enter the tissue to engulf foreign particles
-Cells release cytokines that trigger an immune response in the infected area
Cytokines are cell-signalling compounds that stimulate inflammation and an immune response
-They are small proteins molecules
-Interleukins are a group of cytokines
-Interleukin 1 (IL-1) and interleukin 6 (IL-6) promote inflammation
-IL-1 targets the brain, causing drowsiness and fever
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wound repair
A scab is formed as a result of blood clotting
Underneath this scab, there are stem cells that divide by mitosis to heal the wound
Wound healing occurs in a number of overlapping stages:
-New blood vessels form
Collagen is produced
-Granulation tissue forms to fill the wound
-Stem cells move over the new tissue and divide to produce epithelial cells
-Contractile cells cause wound contraction
-Unwanted cells die
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disadvantages of non specific immune response
Non-specific defences are present in humans from birth. The rapid response is the same for every pathogen; they do not distinguish between pathogens
They are not always effective
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phagocytes structure
Phagocytes are white blood cells that are produced continuously in the bone marrow
They are stored in the bone marrow before being distributed around the body in the blood
They are responsible for removing dead cells and invasive microorganisms
They carry out what is known as a non-specific immune response
There are three main types of phagocyte, each with a specific mode of action.
The three types are:
-Neutrophils
-Macrophages
-Dendritic cells
As they are all phagocytes, they carry out phagocytosis (the process of recognising and engulfing a pathogen) but the process is slightly different for each type of phagocyte
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neutrophils
Neutrophils travel throughout the body and often leave the blood by squeezing through capillary walls to ‘patrol’ the body tissues
During an infection, they are released in large numbers from their stores
However, they are short-lived cells
They have a lobed nucleus which can be used to identify them in blood smears
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neutrophils mode of action
Chemicals released by pathogens, as well as chemicals released by the body cells under attack (eg. histamine), attract neutrophils to the site where the pathogens are located (this response to chemical stimuli is known as chemotaxis)
Neutrophils move towards pathogens (which may be covered in antibodies)
The antibodies are another trigger to stimulate neutrophils to attack the pathogens (neutrophils have receptor proteins on their surfaces that recognise antibody molecules and attach to them)
Once attached to a pathogen, the cell surface membrane of a neutrophil extends out and around the pathogen, engulfing it and trapping the pathogen within a phagocytic vacuole
This part of the process is known as endocytosis
The neutrophil then secretes digestive enzymes into the vacuole (the enzymes are released from lysosomes which fuse with the phagocytic vacuole)
These digestive enzymes destroy the pathogen
After killing and digesting the pathogens, the neutrophils die
Pus is a sign of dead neutrophils
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macrophages
Macrophages are larger than neutrophils and are long-lived cells
Rather than remaining in the blood, they move into organs including the lungs, liver, spleen, kidney and lymph nodes
After being produced in the bone marrow, macrophages travel in the blood as monocytes, which then develop into macrophages once they leave the blood to settle in the various organs listed above
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macrophages mode of action
Macrophages play a very important role in initiating an immune response
Although they still carry out phagocytosis in a similar way to neutrophils, they do not destroy pathogens completely
They cut the pathogens up so that they can display the antigens of the pathogens on their surface (through a structure called the major histocompatibility complex)
These displayed antigens (the cell is now called an antigen-presenting cell) can then be recognised by lymphocytes (another type of white blood cell)
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dendritic cells
Dendritic cells are large phagocytic cells with lengthy extensions
These extensions give them a large surface area to interact with pathogens and lymphocytes
These cells can be found throughout the body
Once they have ingested foreign material they transport it to the lymph nodes
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the role of antigen presenting cells
T-lymphocytes produce an immune response when they are exposed to a specific antigen
T cells will only bind to an antigen if it is present on the surface of an antigen-presenting cell
These cells present the antigens from toxins, foreign cells and ingested pathogens
They help to recruit other cells of the immune system to produce a specific immune response
An antigen-presenting cell is one of the host's cells
It might be a macrophage or a body cell that has been invaded by a pathogen and is displaying the antigen on its cell surface membrane
Once the surface receptor of the T cell binds to the specific complementary antigen it becomes sensitised and starts dividing to produce a clone of cells
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phagosome
The vacuole formed around a bacterium once it has been engulfed by a phagocyte is called a phagosome. A lysosome fuses with the membrane of the phagosome (to form a phagolysosome) and releases lysozymes (digestive enzymes) to digest the pathogen.
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blood smears
A blood smear is when a small amount of blood is spread on a glass microscope slide, stained and covered with a coverslip
The different blood cells can then be examined using a microscope
Red blood cells have no nuclei and a distinct biconcave shape
White blood cells have irregular shapes
Neutrophils have distinctive lobed nuclei
They make up roughly 70% of all white blood cells
Lymphocytes have very large nuclei that nearly occupy the entire cell
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third line of defence
Lymphocytes and antibodies provide the third line of defence against pathogens
Unlike the first and second lines of defence, the third line is specific
Specific immune responses are slower but more effective than non-specific immune responses
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lymphocytes
Lymphocytes are:
-A type of white blood cell
-Smaller than phagocytes
-Have a large nucleus that fills most of the cell
-Produced in the bone marrow before birth
-Travel around the body in the blood
There are two types of lymphocytes (with different modes of action)
T-lymphocytes (T cells)
Lymphocytes that mature in the thymus gland
B-lymphocytes (B cells)
Lymphocytes that mature in the bone marrow
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maturation of T-lymphocytes
Immature T-lymphocytes originate in the bone marrow
They move to the thymus gland in the chest, which is where they mature
During the process of maturation T lymphocytes (T cells) gain specific cell surface receptors called T cell receptors (TCRs)
These receptors have a similar structure to antibodies and are each complementary to a different antigen
A small number of T cells have the same TCRs, these genetically identical cells are called clones
T cells within each clone differentiate into different types of T cell: T helper cells, T killer cells and T regulator cells
There is a very large number of different T cells with different TCRs
This variation allows the T cells to recognise a wide range of foreign antigens
Foreign antigens can be found on the surface of microorganisms, their cell products and toxins
The matured T cells remain inactive until they encounter their specific antigen
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antigen presentation
Macrophages engulf pathogens and present the pathogen antigens on their own cell surface membrane
They become antigen-presenting cells (APCs)
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clinal selection
T cells with T cell receptors that are complementary to the specific pathogenic antigen bind to the APC
They are the clones that have been selected for replication
Binding to the complementary antigens causes the T cell to be activated
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clinal expansion
Activated T cells divide by mitosis to produce clones
There are now many T cells in the blood, all of which have specific roles
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t helper cells
These cells release chemical signalling molecules known as interleukins (a type of cytokines)
Interleukins causes phagocyte activity to increase
Interleukins is needed to activate B cells
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t killer cells
T killer cells patrol the body in search of antigen-presenting body cells
T killer cells attach to the foreign antigens on the cell surface membranes of infected cells and secrete toxic substances that kill the infected body cells, along with the pathogen inside
Perforins secreted by T killer cells punch a hole in the cell surface membrane of infected cells, allowing toxins to enter
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t regulatory cells
Without checks the immune system can spiral out of control and cause serious damage to the host
T regulator cells down-regulate the host immune response by:
Preventing T cells from attacking and killing uninfected host cells
Shutting down the immune system once the body is cleared of the pathogen
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t memory cells
Memory cells remain in the blood, meaning that if the same antigen is encountered again the process of clonal selection will occur much more quickly
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maturation of b lymphocytes
B-lymphocytes (B cells) remain in the bone marrow until they are mature and then spread through the body, concentrating in lymph nodes and the spleen
During the process of maturation B cells gain specific cell surface receptors called B cell receptors (BCRs)
The receptors on the cell surface of B cells are antibodies and are sometimes referred to as antibody receptors
Part of each antibody molecule forms a glycoprotein receptor that can combine specifically with one type of antigen
A small number of B cells have the same BCRs, these genetically identical cells are called a clone
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clinal selection and activation ; b cells
B cells with complementary antibody receptors bind to antigens on antigen presenting cells; this is clonal selection
These antigen presenting cells can be phagocytes, infected cells, or the pathogens themselves
This binding, together with interleukins released by T helper cells activates the B cel
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clonal expansion ; b cells
Activated B cells divide by mitosis to produce clones
This results in large numbers of identical B-lymphocytes being produced over a few weeks
Some of these B-lymphocytes differentiate into plasma cells
Plasma cells secrete lots of antibody molecules (specific to the antigen) into the blood, lymph or linings of the lungs and the gut
The other B-lymphocytes become memory cells that remain circulating in the blood for a long time
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memory cells
During clonal expansion T and B cells form memory cells
Memory cells form the basis of immunological memory – the cells can last for many years and often a lifetime
There are two types of immune response:
Primary immune response (responding to a newly encountered antigen)
Secondary immune response (responding to a previously encountered antigen)
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the primary immune response
The primary immune response has a considerate time delay
It takes considerable energy and time for:
-The clonal selection and expansion of specific T cells and B cells
-The synthesis of antibodies
Antibodies do not begin to appear in the blood until roughly 10 to 17 days after the foreign antigen first entered the body
This time delay is why we often experience symptoms of a disease when we are first exposed to a pathogen
Some of the B cells differentiate during clonal expansion to become plasma cells and memory cells
Plasma cells are short-lived
A portion of the selected T cells also differentiate into memory cells
Memory cells remain circulating in the blood for a long time and allow for a rapid secondary immune response
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b memory cells and the secondary immune response
If the same foreign antigen is found in the body a second time, the B memory cells recognise the antigen
B memory cells divide very quickly and differentiate into plasma cells (to produce antibodies) and more memory cells
This response is very quick, meaning that the infection can be destroyed and removed before the pathogen population increases too much and symptoms of the disease develop
This response to a previously encountered pathogen is, relative to the primary immune response, extremely fast
The response is quicker because there are more memory cells present to be selected than there were cells within the original clone (that existed prior to the first infection)
More memory cells can be selected and so more antibodies are produced within a short time period
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t memory cells and the secondary immune response
T-lymphocytes also play a part in the secondary immune response
They differentiate into memory cells, producing two main types:
Memory helper T cells
Memory killer T cells
Just like the memory cells formed from B-lymphocytes, these memory T cells remain in the body for a long time and provide long-term immunity
If the same antigen is found in the body a second time, these memory T cells become active very quickly
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structure of antibodies
Antibodies are globular glycoproteins called immunoglobulins
Antibodies have a quaternary structure (which is represented as Y-shaped), with two ‘heavy’ (long) polypeptide chains bonded by disulfide bonds to two ‘light’ (short) polypeptide chains
Each polypeptide chain has a constant region and variable region
The constant regions do not vary within a class (isotype) of antibodies but do vary between the classes. The constant region determines the mechanism used to destroy the antigens
There are 5 classes of mammalian antibodies each with different roles
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structure of antibodies p2
The amino acid sequence in the variable regions of the antibodies (the tips of the "Y") are different for each antibody. The variable region is where the antibody attaches to the antigen to form an antigen-antibody complex
At the end of the variable region is a site called the antigen-binding site. Each antigen-binding site is generally composed of 110 to 130 amino acids and includes both the ends of the light and heavy chains
The antigen-binding sites vary greatly giving the antibody its specificity for binding to antigens.
The sites are specific to the epitope (the part of the antigen that binds to the antibody)
A pathogen or virus may therefore present multiple antigens meaning different antibodies need to be produced
The ‘hinge’ region (where the disulfide bonds join the heavy chains) gives flexibility to the antibody molecule which allows the antigen-binding site to be placed at different angles when binding to antigens
This region is not present in all classes of antibodies
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function of antibodies
Antibodies are produced by B-lymphocytes
Antibodies bind to specific antigens that trigger the specific immune response. Every antigen has one antibody
Antigens include pathogens and their toxins, pollen, blood cell surface molecules and the surface proteins found on transplanted tissues
The function of antibodies is to destroy pathogens within the body either directly, or by recruiting other immune cells
Antibodies can act as anti-toxins, opsonins and agglutinins
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antibodies as antitoxins
The way in which antibodies function can vary
Antibodies can combine with viruses and toxins of pathogens (e.g. bacteria) to block them from entering or damaging cells
Antibodies can act as anti-toxins by binding to toxins produced by pathogens (e.g. the bacteria that cause diphtheria and tetanus) which neutralises them making them harmless
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antibodies (opsonisation)
Antibodies can attach to bacteria making them readily identifiable to phagocytes, this is called opsonisation.
Once identified, the phagocyte has receptor proteins for the heavy polypeptide chains of the antibodies, which enables phagocytosis to occur
Antibodies can attach to the flagella of bacteria making them less active, which makes it easier for phagocytes to do phagocytosis
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antibodies as agglutinins
Antibodies act as agglutinins causing pathogens carrying antigen-antibody complexes to clump together (agglutination).
This reduces the chance that the pathogens will spread through the body and makes it possible for phagocytes to engulf a number of pathogens at one time
Antibodies (together with other molecules) can create holes in the cell walls of pathogens causing them to burst (lysis) when water is absorbed by osmosis
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active immunity
Active immunity is acquired when an antigen enters the body triggering a specific immune response (antibodies are produced)
Active immunity is naturally acquired through exposure to microbes or artificially acquired through vaccinations
The body produces memory cells, along with plasma cells, in both types of active immunity giving the person long-term immunity
In active immunity, during the primary response to a pathogen (natural) or to a vaccination (artificial), the antibody concentration in the blood takes one to two weeks to increase.
If the body is invaded by the same pathogen again or by the pathogen that the person was vaccinated against then, during the secondary response, the antibody concentration in the blood takes a much shorter period of time to increase and is higher than after the vaccination or first infection
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passive immunity
Passive immunity is acquired without an immune response. Antibodies are not produced by the infected person
As the person’s immune system has not been activated then there are no memory cells that can produce antibodies in a secondary response. If a person is reinfected they would need another infusion of antibodies
Depending on the disease a person is infected with (eg. tetanus) they may not have time to actively acquire the immunity, that is, there is no time for active immunity. So passive immunity occurs either artificially or naturally
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artificial passive immunity
Artificial passive immunity occurs when people are given an injection / transfusion of the antibodies. In the case of tetanus this is an antitoxin.
The antibodies were collected from people whose immune system had been triggered by a vaccination to produce tetanus antibodies
Natural passive immunity occurs when:
Foetuses receive antibodies across the placenta from their mothers
Babies receive the initial breast milk from mothers (the colostrum) which delivers a certain isotype of antibody (IgA)
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autoimmune diseases
Roughly 5% of the British population suffer from an autoimmune disease
An autoimmune disease occurs when the body attacks itself
The immune system damages cells of the body as a result
Antibodies, T cells (helper and cytotoxic) and B cells attack one or more self-antigens
Glycoproteins and glycolipids form surface antigens that enable the immune system to determine whether the cell belongs to the body or if it is foreign
The attack can be targeted towards a single organ or it can be directed towards the entire body
Systemic lupus erythematosus (SLE) is an example of an autoimmune disease that affects several organs
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lupus
Lupus is a notoriously hard disease to diagnose as the symptoms that individual present with often vary drastically
The most distinctive symptom of lupus is a butterfly rash across the face
Women tend to suffer from the disease more than men
The connective tissue of the body is attacked by the immune system, affecting several organs
Areas affected include the joints, kidneys, heart, lungs and skin
It causes long-term destruction
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rheumatoid arthritis
Rheumatoid arthritis is an autoimmune disease that solely affects the joints
It is different from osteoarthritis in several ways
It usually begins in the fingers and hands, spreading to the shoulders and elsewhere
Symptoms include muscle spasms, inflamed tendons, lethargy and constant joint pain
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causes of autoimmune diseases
The causes of autoimmune diseases are still not fully understood
There is a lot of research currently underway in this field
Scientists have deduced that genetics is an influencing factor
Susceptibility to an autoimmune disease was shown to be inherited
Susceptibility is the likelihood of an individual developing the disease when exposed to the specific pathogen or stimulus
However, research has also suggested that the environment is also important
When individuals moved from areas of low autoimmune disease prevalence (like Japan) to areas of higher autoimmune disease prevalence (like the USA) they showed an increased chance of developing an autoimmune disease
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principles of vaccinations
The principles underpinning vaccinations were discovered by Edward Jenner in the 1700s when he developed the first smallpox vaccine
A vaccine is a suspension of antigens that are intentionally put into the body to induce artificial active immunity. A specific immune response where antibodies are released by plasma cells
There are two main types of vaccines:
Live attenuated
Inactivated
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how are vaccines administered
Vaccines are administered either by injection or orally (by mouth)
The vaccinations given by injection can be into a vein or muscle
Vaccinations produce long-term immunity as they cause memory cells to be created. The immune system remembers the antigen when reencountered and produces antibodies to it, in what is a faster, stronger secondary response
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vaccination programs in countries
Vaccination programmes are offered to citizens by the government as a major component of health protection
The young in the population are given vaccines to protect them from diseases that were once common and caused serious harm
For example, in the UK babies are vaccinated against polio and measles
A country may not have had any cases of a particular disease for several years however international travel means there is the possibility that a disease could be reintroduced at any time by travellers coming from other countries
By having their citizens vaccinated against diseases governments can prevent serious epidemics from occurring
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effectiveness of vaccine
Very few drugs are effective against viruses which is why vaccines are critical in controlling the spread of viruses
Vaccines can be:
Highly effective with one vaccination giving a lifetime’s protection (although less effective ones will require booster / subsequent injections)
Generally harmless as they do not cause the disease they protect against because the pathogen is killed by the primary immune response
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problems with vaccines
Unfortunately, there can be problems with vaccines due to:
People having a poor response (eg. they are malnourished and cannot produce the antibodies – proteins or their immune system may be defective)
Antigenic variation – the variation (due to major changes) in the antigens of pathogens causes the vaccines to not trigger an immune response or diseases caused by eukaryotes (eg. malaria) have too many antigens on their cell surface membranes making it difficult to produce vaccines that would prompt the immune system quickly enough
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how do virususechange their surfaces
Viruses having the capacity to change their surface antigens (the targets of vaccines) by:
Antigenic drift – over time there are small changes in the structure and shape of antigens (within the same strain of virus)
Antigenic shift – there are major changes in antigens (within the same strain of virus)
Antigenic concealment – the pathogen ‘hides’ from the immune system by:
-Living inside cells
-Coating their bodies in host proteins
-Parasitising immune cells such as macrophages and T cells (eg. HIV)
-Remaining in parts of the body that are difficult for vaccines to reach (eg. Vibrio cholerae – cholera, remains in the small intestine)
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cross breeding in viruses
Cross-breeding – different strains of the virus invade the same cell, producing new viruses with antigens from different strains (essentially the strains swap antigens with each other)
The strains of influenza viruses that cause human influenza have been known to crossbreed with viruses that cause similar diseases in other animals
This crossbreeding can produce new strains of the human influenza virus that cause pandemics (as no individuals have immunity against them)
Every year the World Health Organisation (WHO) tries to provide information about strains that are likely to spread in order to aid government decisions and the development of flu vaccines
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herd immunity
Herd immunity arises when a sufficiently large proportion of the population has been vaccinated (and are therefore immune) which makes it difficult for a pathogen to spread within that population
Those who are not immunised are protected and unlikely to contract it as the levels of the disease are so low
It is very important as it allows for the individuals who are unable to be vaccinated (e.g. children and those with weak immune systems) to be protected from the disease
The proportion of the population that needs to be vaccinated in order to achieve herd immunity is different for each disease
Governments will often vaccinate as many people as possible
If vaccination rates fall below the required level then herd immunity can break down
There was an outbreak of Measles in Swansea in 2012 due to a lack of vaccine uptake
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ring immunity
Ring immunity is another way by which mass vaccination programmes can work
People living or working near a vulnerable (or infected) person are vaccinated in order to prevent them from catching and transmitting the disease
The vaccinated individuals do not spread the pathogen onto others so those vulnerable individuals "within the ring" are protected as the people they interact with will not have the disease
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the challenges of eradicating disease
Eradicating disease presents a challenge
On one hand some pathogens are simply complicated and present with disease processes that are not straightforward and so a successful vaccine has not been developed
On the other hand, diseases that could be eradicated where a vaccine does exist, have not been eliminated because too few in the community have been vaccinated
It has also been difficult to eradicate other infectious diseases due to:
Unstable political situations in areas such as Africa, Latin America and parts of Asia, perhaps resulting in civil unrest or wars
Lack of public health facilities (poor infrastructure, few trained personnel, limited financial resources)
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live attenuated vaccines
Live attenuated vaccines contain whole pathogens (e.g. bacteria and viruses) that have been ‘weakened’
These weakened pathogens multiply slowly allowing for the body to recognise the antigens and trigger the primary immune response (plasma cells to produce antibodies)
These vaccines tend to produce a stronger and longer-lasting immune response
They can be unsuitable for people with weak immune systems as the pathogen may divide before sufficient antibodies can be produced
An example of this type of vaccine is the MMR (Measles, Mumps and Rubella)
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inactive vaccines
Inactivated vaccines contain whole pathogens that have been killed (‘whole killed’) or small parts (‘subunit’) of the pathogens (eg. proteins or sugars or harmless forms of the toxins – toxoids)
As inactivated vaccines do not contain living pathogens they cannot cause disease, even for those with weak immune systems
However, these vaccines do not trigger a strong or long-lasting immune response like live attenuated vaccines. Repeated doses and/or booster doses are often required
Some people may have allergic reactions or local reactions (eg. sore arm) to inactivated vaccines as adjuvants (eg. aluminium salts) may be conjugated (joined) to the subunit of the pathogen to strengthen and lengthen the immune response
An example of a whole killed vaccine is the polio vaccine
An example of a toxoid subunit vaccine (where inactivated versions of the toxins produced by pathogens are used) is Diphtheria
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eradication of small pox
The eradication of Smallpox is a success story, but its success had specific reasons that cannot be universally replicated in the struggle to eliminate disease
Smallpox is a highly contagious disease caused by a virus that exists in two forms: Variola minor and Variola major, the latter being the worst of the two, with a death rate of 12 to 30%
Smallpox was transmitted by direct contact and caused red spots (which filled with pus) to cover the body. People who recovered were disfigured as a result of scabs that formed from these spots. It also affected the eyes resulting in permanent blindness for many who recovered
The WHO began an eradication programme against smallpox in 1967, stating their intention to eradicate the virus within ten years. The WHO did not declare smallpox eradicated until 1980
The programme focused on:
Vaccination – the aim was to vaccinate more than 80% of populations at risk and if a case of smallpox was reported ring vaccination would occur (where everyone in the household with the reported case, the surrounding 30 households, relatives and anyone else who had contact would get vaccinated)
Surveillance
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discovering new drugs
The worrying increase of antibiotic-resistant bacteria strains means that scientists are always looking for new antibiotics
A lot of time and money is required to successfully develop a drug. There are several trials that a drug must pass before being approved by a national regulatory authority
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ways in which new drugs are developed
There are several different ways in which new drugs are discovered and developed:
The analysis of an organism's genome to find candidate genes that may code for potential drugs
Identifying molecules that fit into drug targets e.g. receptors and hormones or neurotransmitters and synapses
Modifying drugs that already exist (this is done by using computer programmes that model the molecular structures of drugs and target molecules)
Identification of useful compounds produced by organisms (e.g. fungi, plants, animals and actinobacteria)
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bacteria and fungi as sources of medicine
Bacteria and fungi have provided many antibiotics
Quite recently compounds called rifamycins have been discovered in marine actinobacteria. These compounds kill bacteria by inhibiting bacterial transcription
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plants as a source of medicine
Plants have been a major source of drugs for hundreds of years
Artemisinin is a drug found in Sweet wormwood and it treats malaria by killing the pathogen while it is in the red blood cells
Quinidine is derived from the Quinine tree and it treats a fast heart rate by blocking channel proteins in cardiac muscle to reduce impulse conduction
Many plants are used in traditional Chinese medicine, scientists are keen to catalogue and study these plants to see what drugs they can provide
Continued access to these drugs and the discovery of new drugs is a strong argument for maintaining biodiversity at a global level
Microorganism and plant species may go extinct before we have the chance to discover what drugs they can provide
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personalised medicine
Currently, a "one type fits all" attitude is applied when prescribing drugs to individuals with the same disease or condition
Personalised medicine involves the development of more targeted and personalised drugs to treat a variety of human diseases as well as the development of synthetic tissues
For example, the drug isoniazid is used to treat TB. Some individuals metabolize the drug slowly (making it effective at treating the disease) while others metabolize it much faster (making it an ineffective treatment)
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genomic medicine
Information gathered from genome projects like the Human Genome Project (HGP) can be used to develop genomic medicine
Genomic medicine uses information about an individuals genes to influence their clinical care
Ideally, doctors could prescribe the most effective drugs for an individual based on their genome
Between individuals, there are differences in DNA base sequences. These differences can affect the tertiary structure of the proteins which are targeted by drugs
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testing for genetically modified medicine
The information gained from genetic testing could be used to divide the population into subgroups according to how they are likely to respond to specific drugs. This would ensure that individuals receive the most effective drugs that cause the least side effects
Serious progress has been made in personalised cancer medicine
Herceptin is an antibody drug used to treat some breast cancers, it affects a specific cell surface receptor. A patient is only given the drug if they are found to have high numbers of this receptor
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genetic screening
Genetic screening is also a form of personalised medicine as it allows for individuals with a high chance of developing specific diseases to be identified and for preventative measures or precautions to be taken
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synthetic biology
Synthetic biology is a recent area of research that aims to create new biological parts, devices, and systems, or to redesign systems that already exist in nature
It is much more complex than genetic engineering as it involves assembling an entire genome. This genome can cause a cell to operate in a novel way, not yet seen before
The assembly of the genome can be done using known existing DNA sequences or by using entirely new sequences
These new sequences can be written (using special computer programmes) so that they produce specific proteins or transcription factors
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producing artemisinin
The most well-known use of synthetic biology is the commercial production of artemisinin
Artemisinin is an antimalarial drug that is difficult to produce in other ways
E.coli and yeast are completely genetically reprogrammed so that they produce the precursor of the drug on a large scale
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antibiotics
When humans experience a pathogenic bacterial infection they are often prescribed antibiotics by a healthcare professional
Antibiotics are chemical substances that inhibit or kill bacterial cells with little or no harm to human tissue
Many antibiotics are derived from naturally occurring substances that are harmful to prokaryotic cells (structurally or physiologically) but usually do not affect eukaryotic cells
The aim of antibiotic use is to aid the body’s immune system with fighting a bacterial infection
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different types of antibiotics
Antibiotics are either described as being bactericidal (they kill) or bacteriostatic (they inhibit growth processes), they target prokaryotic features but can affect both pathogenic and mutualistic bacteria living on or in the body
Some antibiotics are derived from fungi while others are synthetic or semi-synthetic
Broad-spectrum antibiotics act on a wide range of bacteria while narrow-spectrum antibiotics act on a very small number of bacteria
Doctors often prescribe broad-spectrum antibiotics (e.g. Amoxicillin) unless a culture has been taken to prove the need for a narrow-spectrum antibiotic
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genetic biodiversity on antibiotics
In all species, there exists genetic diversity within populations, and the same applies to disease-causing bacteria
Individual bacterial cells may possess alleles that confer resistance to the effects of the antibiotic
These alleles are generated through random mutation and are not caused by antibiotic use, but antibiotic use exerts selection pressures that can result in an increase in their frequency
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bacterial dna
Bacteria have a single loop of DNA with only one copy of each gene so when a new allele arises it is immediately displayed in the phenotype
When an antibiotic is present:
-Individuals with the allele for antibiotic resistance have a massive selective advantage so they are more likely to survive, reproduce and pass genome (including resistance alleles)
-Those without alleles are less likely to die and reproduce
-Over several generations, the entire population of bacteria may be antibiotic-resistant
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antibiotic resistance
Antibiotic resistance is an important example of natural selection
Some pathogenic bacteria have become resistant to penicillin as they have acquired genes that code for the production of the enzyme β-lactamase (also known as penicillinase), which breaks down penicillin
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reasons for antibiotic resistance
Overuse of antibiotics and antibiotics being prescribed when not necessary
Large scale use of antibiotics in farming to prevent disease when livestock are kept in close quarters, even when animals are not sick
Patients failing to complete the full course of antibiotics prescribed by doctors
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consequences of antibiotic resistance
These factors have led to a reduction in the effectiveness of antibiotics, and an increase in the incidence of antibiotic resistance
Bacteria living where there is widespread use of many different antibiotics may have plasmids containing resistance genes for several different antibiotics, giving them multiple resistance and presenting a significant problem for doctors
In addition, resistance may first appear in a non-pathogenic bacterium, but then be passed on to a pathogenic species by horizontal transmission
There is a constant race to find new antibiotics as resistant strains are continuously evolving
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staphylococcus aureus
The most common example of a resistant bacteria is a strain of Staphylococcus aureus that has developed resistance to a powerful antibiotic, methicillin and is now known as MRSA (Methicillin-resistant Staphylococcus aureus)
Some MRSA strains have also become resistant to other antibiotics (eg. penicillin)
S.aureus usually lives on human skin,
without causing disease however when there is an opportunity for the pathogen to enter the body (e.g. surgical wound) they can cause serious disease
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clostridium difficile
Clostridium difficile is a bacteria present in the human gut
The numbers of C.diff are usually kept low due to the presence of other gut bacteria
A course of antibiotics can kill these 'friendly' gut bacteria, allowing C.diff to increase in numbers
A C.diff infection can cause diarrhoea and fever as they disrupt the epithelium of the intestine
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prevention of antibiotic resistance
Tighter controls in countries in which antibiotics are sold without a doctor’s prescription
Doctors avoiding the overuse of antibiotics, prescribing them only when needed (patients must only be given antibiotics when absolutely essential) – doctors should test the bacteria first to make sure that they prescribe the correct antibiotic
Antibiotics not being used in non-serious infections that the immune system will ‘clear up’ (patients must not keep unused antibiotics for self-medication of such non-serious infections in the future)
When prescribed a course of antibiotics, the patient finishing the entire course (even if they feel better after a few days) so that all the bacteria are killed, and none are left to mutate to become resistant strains
Antibiotics not being used for viral infections (antibiotics have no effect on viruses anyway, and this just provides an unnecessary chance for bacteria to develop resistance)
The use of ‘wide-spectrum’ antibiotics being reduced and instead those antibiotics that are highly specific to the infection (‘narrow-spectrum’ antibiotics) being used
The type of antibiotics prescribed being changed so that the same antibiotic is not always prescribed for the same infections and diseases (this reduces the chance of a resistant strain developing)
The use of antibiotics being reduced and more tightly controlled in industries such as agriculture – controls are now in place to limit their use in farming, where antibiotics are used to prevent, rather than cure, bacterial infections
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limiting the spread of already resistant strains
The spread of already-resistant strains can be limited by:
Ensuring good hygiene practices such as handwashing and the use of hand sanitisers (this has reduced the rates of resistant strains of bacteria, such as MRSA, in hospitals)
Isolating infected patients to prevent the spread of resistant strains, in particular in surgical wards where MRSA can infect surgical wounds
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conjugation
dna is transferred between bacteria horizontally through pili
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transformation
bacterium take up dna floating in its environment from dead bacterium
