Communicable Diseases, Disease Prevention & the Immune System (OCR A Level Biology): Flashcards

• The viral enzyme reverse transcriptase produces single-stranded DNA from the viral RNA

• DNA polymerase synthesises double-stranded DNA from this single-stranded DNA

• The double-stranded DNA is inserted into the host DNA, where it can remain inactive for many years

• Once activated, the DNA provirus is used to synthesise new viruses

Malaria is caused by a protoctist (protist).

The parasite is spread by (female) mosquitoes. Infected individuals experience fever, chills and fatigue.

Late blight is caused by a protoctist (unusually, it has some fungal characteristics).

It is transmitted via spores. The first signs are small, dark brown marks on the leaves that quickly increase in size and number, and it destroys potato and tomato crops, leaving them inedible.

Like plants, fungi are eukaryotic with cell walls and large central vacuoles.

However, instead of separate cells, their bodies consist of filaments called hyphae, which form a network that spreads throughout a host or the soil.

Black Sigatoka is caused by a fungus.

It spreads through the leaves, reducing the plant's ability to photosynthesise. The lack of photosynthesis causes parts of the leaf to die, producing black streaks, until eventually the whole leaf dies.

Athlete's foot is a fungal disease that exists on the surface of the skin, transmitted by skin-to-skin contact.

Non-pathogenic bacteria do not cause disease or damage, whereas pathogenic bacteria cause disease. Pathogenic bacteria do not always infect host cells; they can remain within body cavities or spaces.

False — viruses have no cellular structure, so they must hijack a host cell's machinery to replicate.

True

The transfer of pathogens from an infected host to an uninfected host.

Pathogens must transfer from host to host to survive; if they cannot find new hosts, the population goes extinct.

Any organism that transfers a pathogen from an infected individual to an uninfected individual.

The vector itself is usually not harmed by the pathogen. Many disease vectors are insects, because they reproduce in large numbers, increasing the likelihood of transmission.

By direct physical contact between individuals.

When the leaves of an infected plant touch the leaves of an uninfected plant, particles of the virus are transmitted.

Through the air via tiny droplets of water.

An infected individual breathes out droplets containing the virus, which are then breathed in by an uninfected individual. Being in close proximity is sufficient for transmission.

Spores are very small reproductive structures that are released into the environment and dispersed by wind or water.

Once they reach a food source (host) they begin growing. For example, P. infestans (potato blight) produces specialised spores called sporangia, adapted for wind dispersal.

Only by the direct exchange of body fluids through intimate human contact (HIV cannot survive outside the human body and is not spread by a vector), for example:

• sexual intercourse

• blood donation / transfusion

• 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

By droplet infection.

Infected people with the active disease cough or sneeze, releasing Mycobacterium tuberculosis into the air in tiny droplets of liquid. Uninfected people then inhale these droplets.

TB therefore spreads more quickly among people living in overcrowded conditions.

It occurs in cattle and is spread to humans through contaminated meat and unpasteurised milk.

This route is now rare in developed countries, but meat and milk can still be a source of infection in some developing countries.

By an insect vector — the female Anopheles mosquito.

The mosquito takes up Plasmodium when feeding on the blood of an infected person, then passes it to a new human when feeding again.

Malaria may also be transmitted by:

• blood transfusion

• re-use of unsterile needles

• from mother to child across the placenta

• The presence of the pathogen — if the pathogen is not present it cannot spread.

• The presence of susceptible individuals — a high proportion of immune or resistant individuals reduces the likelihood of transmission.

Resistance: the individual has genetically-coded mechanisms that prevent infection or spread of the pathogen. On first exposure they develop no disease and no symptoms (e.g. sickle cell heterozygotes resist malaria).

Immunity: the individual has been previously infected, suffered symptoms and recovered. They are highly unlikely to develop symptoms if exposed again.

Pathogens spread by contact or droplets need hosts in close proximity, so areas of high population density (cities, schools, homeless shelters) have higher infection rates.

• Plasmodium became resistant to the drugs used to control it.

• Anopheles mosquitoes became resistant to DDT and other insecticides used against them.

The Anopheles mosquito also favours habitats with high rainfall, high temperature and high humidity, so malaria remains widespread throughout the tropics and sub-tropics.

A disease that is always present in a population, even if in very low numbers, is described as endemic.

(An epidemic is a large increase in cases/an outbreak; a pandemic is an epidemic that occurs on a large scale and crosses international boundaries.)

Poverty correlates with higher transmission: crowded housing with poor sanitation, no sewage or water treatment and limited hygiene products allow water-borne diseases (e.g. typhoid, cholera, polio) to spread.

False — HIV cannot survive outside the human body and is spread only by direct exchange of body fluids, not by a vector.

True

• Passive defences (always present)

• Active defences (activated when pathogens invade)

Defence mechanisms that are always present in the plant, including physical barriers that prevent pathogen entry and chemicals that reduce or prevent pathogen growth.

Defence mechanisms that are activated once a pathogen has invaded the plant, such as hypersensitivity and the formation of physical barriers by callose.

• Waxy cuticle

• Cellulose cell wall

• Closed stomata

• Bark

• Casparian strip

Only if there is a wound on the leaf surface or stem, commonly caused by grazing herbivores.

They prevent pathogens from growing on the plant surface, often by creating acidic conditions.

Plant cells have cell walls, so substances cannot move freely around the plant as immune cells do in animals.

This makes cell signalling essential for coordinating the active defence response.

The rapid death of tissue surrounding the infection site. Although extreme, it is effective because it deprives pathogens of host tissue, nutrients and energy.

Callose and lignin.

• Forms a matrix in which antimicrobial compounds (hydrogen peroxide and phenols) can be deposited

• Narrows the plasmodesmata, reducing the size of channels between neighbouring cells

• Forms ingrowths into xylem vessels (tyloses)

• Blocks the phloem by filling sieve pores, preventing transport of phloem sap

Pathogens possess cellulase enzymes that digest cellulose in plant cell walls.

The molecules produced act as signals to cell surface receptors, stimulating the release of defence chemicals called phytoalexins.

• Disrupting pathogen metabolism

• Delaying pathogen reproduction

• Disrupting bacterial cell surface membranes

• Stimulating the release of chitinases (enzymes that break down chitin in fungal cell walls)

Salicylic acid is a signalling molecule that migrates to uninfected areas of the plant, activating defences and giving long-term protection known as systemic acquired resistance.

Plants under pathogen attack secrete ethylene onto their leaves.

The ethylene vaporises, stimulating other leaves on the same plant (and other plants) to react.

• Toxic compounds (e.g. catechol)

• Sticky resin in bark that traps pathogens

• Compounds encouraging the growth of competing microorganisms

• Enzyme inhibitors (e.g. tannins)

• Receptor molecules that detect pathogens

Between the cell surface membrane and the cell wall.

False — passive defences are always present; it is active defences that are triggered once a pathogen invades.

True

A defence mechanism present from birth that gives the same rapid response to every pathogen; it does not distinguish between different pathogens.

• Physical – body tissues act as barriers, preventing entry of pathogens

• Cellular – cells detect pathogens, secrete protective substances and ingest/digest pathogens

• Chemical – secreted substances create an inhospitable environment for pathogen growth

• Commensal organisms – harmless bacteria and fungi compete with pathogens for nutrients

It prevents the entry of pathogens into the body.

• Its outer layer is made of dry, dead, hardened cells filled with keratin (a tough fibrous protein), acting as a physical barrier

• Sebum secretions contain fatty acids with antimicrobial properties

• Evaporation of sweat leaves a salt residue; the low moisture, low pH and high salinity create an inhospitable environment for microorganisms

• Mucus-secreting cells (e.g. goblet cells) produce mucus, made sticky by glycoproteins with long carbohydrate chains

• Mucus traps particles such as bacteria, viruses, pollen and dust

• Cilia (hair-like structures) beat in a wave-like manner to move the mucus towards the back of the throat

A cough or sneeze, triggered when a pathogen irritates the lining of an airway.

Antimicrobial enzymes that break down the cell walls of bacteria. They are found in body fluids such as blood, tears, sweat and breast milk.

Hydrochloric acid produced by cells lining the stomach creates a low pH that helps kill bacteria ingested with food.

(Gut cells secrete mucus to protect themselves from the acid.)

Harmless bacteria and fungi (e.g. Candida albicans, E. coli) live on the skin, in the mouth and intestines without causing disease.

They compete with pathogenic microorganisms for nutrients, preventing them from invading host tissue.

The second line of defence involves phagocytic cells and antimicrobial proteins responding to invading pathogens.

• A break in the skin or mucous membranes releases molecules that trigger a chemical cascade

• Platelets release substances that undergo a series of chemical reactions

• Fibrin forms a network that traps platelets, forming a clot

This prevents excess blood loss and pathogen entry, and provides a scab for wound healing.

A local response to infection and tissue damage, causing swelling, warmth and pain.

Small cell-signalling protein molecules that stimulate inflammation and an immune response in the infected area. Interleukins (e.g. IL-1 and IL-6) are a group of cytokines that promote inflammation.

• New blood vessels form

• Collagen is produced and granulation tissue forms to fill the wound

• Stem cells move over the new tissue and divide by mitosis to produce epithelial cells

• Contractile cells cause wound contraction, and unwanted cells die

• Skin

• Mucous membranes

• Expulsive reflexes

• Chemical secretions

It causes a sudden expulsion of air containing respiratory secretions and the foreign particles that have entered the airway.

Mast cells respond to tissue damage by secreting histamine, which stimulates:

• Vasodilation, increasing blood flow through capillaries

• "Leaky" capillaries, allowing fluid into tissues (causing swelling)

• Phagocytes and plasma proteins to leave the blood and enter the tissue

False — non-specific responses give the same rapid response to every pathogen and do not distinguish between them.

True — lysozymes are found in fluids such as tears, sweat, blood and breast milk, where they break down bacterial cell walls.

A white blood cell that carries out phagocytosis, engulfing and destroying dead cells and invasive microorganisms as part of the non-specific immune response.

The process of recognising and engulfing a pathogen.

They are produced continuously in, and stored in, the bone marrow.

• Neutrophils

• Macrophages

• Dendritic cells

Phagocytes are responsible for removing dead cells and invasive microorganisms as part of a non-specific immune response.

The movement of a cell (e.g. a neutrophil) towards a chemical stimulus; chemicals released by pathogens and by body cells under attack (e.g. histamine) attract neutrophils to the site of infection.

• Chemicals from pathogens and from body cells under attack (e.g. histamine) attract the neutrophil to the site by chemotaxis

• Receptor proteins on the neutrophil recognise and attach to antibodies on the pathogen's surface antigens

• The cell surface membrane extends around the pathogen, engulfing it into a phagocytic vacuole

• Lysosomes fuse with the vacuole and release digestive enzymes that destroy the pathogen

• They are short-lived cells that often leave the blood by squeezing through capillary walls to patrol the tissues

• They have a lobed nucleus, which can be used to identify them in blood smears

Dead neutrophils, which die after killing and digesting pathogens.

• Macrophages are larger than neutrophils and are long-lived cells

• They travel in the blood as monocytes, which develop into macrophages once they leave the blood and settle in tissues (e.g. lungs, liver, spleen, kidney, lymph nodes)

Macrophages carry out phagocytosis but do not destroy pathogens completely. Instead they cut the pathogen up and display its antigens on their surface (as part of an MHC), becoming an antigen-presenting cell that can be recognised by lymphocytes. This helps initiate the specific immune response.

Large phagocytic cells with lengthy extensions, giving a large surface area to interact with pathogens and lymphocytes.

One of the host's own cells (e.g. a macrophage, or a body cell invaded by a pathogen) that displays a pathogen's antigen on its cell surface membrane, allowing it to be recognised by T-lymphocytes.

T-lymphocytes will only bind to an antigen when it is presented on the surface of an antigen-presenting cell. Once a T cell's surface receptor binds the specific complementary antigen, it becomes sensitised and divides to produce a clone of cells, helping recruit other immune cells.

They are distributed around the body in the blood.

Once they have ingested foreign material, they transport it to the lymph nodes, where they present antigens to lymphocytes.

False — neutrophils are short-lived; it is macrophages that are long-lived.

True

A line picture which shows specific features that have been observed when a specimen was viewed (e.g. under a microscope).

• A title

• The magnification under which the observations shown were made

• Use a sharp HB pencil on plain white paper

• Lines should be clear, single lines

• No shading

• Draw well-defined structures with proper proportions

• They should not cross one another and should have no arrowheads

• They must connect directly to the part being labelled

• They should be kept to one side, parallel to the top of the page

• They should be drawn with a ruler

So that detail can be shown clearly and the proportions of the structures can be represented accurately.

Cell drawings are typically made when viewing cells at a higher magnification.

Plan drawings are typically made of tissues viewed under lower magnifications, and individual cells are never drawn in a plan diagram.

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.

They have no nuclei and a distinct biconcave shape.

In a blood smear, white blood cells have irregular shapes, whereas red blood cells have a distinct biconcave shape.

A distinctive lobed nucleus.

Lymphocytes have very large nuclei that nearly occupy the entire cell.

You must only ever draw what you see, and not what you think you see.

The eyepiece graticule.

False — individual cells are never drawn in a plan diagram; plan drawings show tissues only.

True

A type of white blood cell that provides the specific (third line of) immune response. Lymphocytes are smaller than phagocytes and have a large nucleus that fills most of the cell.

The specific immune response is slower but more effective than non-specific immune responses.

• T-lymphocytes (T cells) mature in the thymus gland\n\n- B-lymphocytes (B cells) mature in the bone marrow

• Immature T-lymphocytes originate in the bone marrow\n\n- They move to the thymus gland in the chest, where they mature\n\n- During maturation they gain specific cell surface receptors called T cell receptors (TCRs), each complementary to a different antigen

A specific cell surface receptor gained by T cells during maturation. TCRs have a similar structure to antibodies and each is complementary to a different antigen, allowing T cells to recognise a wide range of foreign antigens.

A small number of T cells share the same T cell receptors; these genetically identical cells are called clones.

A cell, such as a macrophage that has engulfed a pathogen, which displays the pathogen's antigens on its own cell surface membrane so they can be recognised by T cells.

• T cells with T cell receptors that are complementary to the specific pathogenic antigen bind to the APC\n\n- These are the clones selected for replication\n\n- Binding to the complementary antigen causes the T cell to be activated

Activated T cells divide by mitosis to produce clones. This produces many T cells in the blood, each with a specific role.

T helper cells release chemical signalling molecules called interleukins (a type of cytokine), which:\n\n- Cause phagocyte activity to increase\n\n- Activate B cells

• They patrol the body and attach to the foreign antigens on the cell surface membranes of infected cells\n\n- They secrete toxic substances that kill the infected cell and the pathogen inside\n\n- Perforins punch a hole in the cell surface membrane, allowing toxins to enter

T memory cells remain in the blood, so that if the same antigen is encountered again, clonal selection occurs much more quickly, giving a faster response.

Proteins secreted by T killer cells that punch a hole in the cell surface membrane of infected cells, allowing toxic substances to enter and destroy the cell.

True

False — it is T helper cells that release interleukins to activate B cells; T killer cells destroy infected body cells using perforins and toxic substances.

White blood cells that mature in the bone marrow and carry out the antibody-mediated (humoral) part of the specific immune response.

They remain in the bone marrow until they are mature.

They gain specific cell surface receptors called B cell receptors (BCRs).

Part of each antibody molecule forms a glycoprotein receptor that combines specifically with one type of antigen.

A small number of B cells that carry the same B cell receptors and are therefore genetically identical.

B cells with complementary antibody receptors bind to antigens on antigen-presenting cells.

This binding is clonal selection.

• Phagocytes

• Infected cells

• The pathogens themselves

• Binding of the B cell's antibody receptor to the antigen

• Interleukins released by T helper cells

Activated B cells divide by mitosis to produce clones, giving large numbers of identical B-lymphocytes over a few weeks.

Activated B-lymphocytes divide by mitosis to produce clones of identical cells.

Plasma cells secrete large numbers of antibody molecules (specific to the antigen) into the blood, lymph, or linings of the lungs and gut.

A differentiated B-lymphocyte that secretes large numbers of antibody molecules specific to the antigen into the blood, lymph or linings of the lungs and gut.

Some activated B-lymphocytes become memory cells that remain circulating in the blood for a long time.

They spread through the body, concentrating in the lymph nodes and the spleen.

They are antibodies, sometimes called antibody receptors.

Memory cells remain circulating in the blood for a long time.

False — B-lymphocytes mature in the bone marrow; it is T-lymphocytes that mature in the thymus.

True

T and B cells formed during clonal expansion that form the basis of immunological memory, remaining in the blood for many years (often a lifetime) to allow a rapid secondary immune response.

The ability, made possible by memory cells, to mount a rapid response to a previously encountered antigen; the reason catching certain diseases twice is so unlikely.

The immune response that occurs when the body responds to a newly encountered antigen for the first time.

The immune response that occurs when the body responds to a previously encountered antigen.

It takes considerable time and energy for:

• The clonal selection and expansion of specific T cells and B cells

• The synthesis of antibodies

Because of the time delay in the primary immune response, antibodies do not begin to appear in the blood until roughly 10 to 17 days after the antigen first enters the body, allowing the pathogen population to increase and cause symptoms.

Some B cells differentiate into:

• Plasma cells, which are short-lived

• Memory cells, which remain circulating in the blood for a long time and allow a rapid secondary immune response

If the same foreign antigen is found in the body a second time, the B memory cells recognise the antigen.

They divide very quickly and differentiate into plasma cells (to produce antibodies) and more memory cells.

This allows the infection to be destroyed and removed before the pathogen population increases too much and symptoms develop.

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, so more antibodies are produced within a short time period.

T-lymphocytes differentiate into:

• Memory helper T cells

• Memory killer T cells

These remain in the body for a long time and provide long-term immunity, becoming active very quickly if the same antigen is encountered again.

During the primary immune response, antibodies do not begin to appear in the blood until roughly 10 to 17 days after the foreign antigen first enters the body.

Memory cells remain circulating in the blood for a long time and allow for a rapid secondary immune response.

Measles has only one strain, so re-infection triggers a very fast secondary immune response and the person does not become ill.

The common cold and influenza are caused by viruses constantly developing into new strains; as each strain has different antigens, a primary immune response (during which we often become ill) must be carried out each time before immunity is achieved.

True

False — antibodies do not begin to appear until roughly 10 to 17 days after the antigen first enters the body.

• Y-shaped molecule with a quaternary structure

• Two heavy (long) polypeptide chains bonded by disulfide bonds to two light (short) polypeptide chains

• Each chain has a constant region and a variable region

Disulfide bonds.

It does not vary within a class (isotype) of antibodies but varies between classes.

It determines the mechanism used to destroy the antigens.

The amino acid sequence of the variable region (the tips of the "Y") differs for each antibody.

This forms an antigen-binding site whose shape is complementary to one specific epitope, so the antibody binds to only one antigen.

The site at the end of each variable region (formed from both the light and heavy chain ends) that is specific to one epitope, allowing the antibody to bind its antigen and form an antigen-antibody complex.

The specific part of an antigen that binds to the antigen-binding site of an antibody.

The hinge region (where the disulfide bonds join the heavy chains) gives the molecule flexibility.

This allows the antigen-binding sites to be placed at different angles when binding to antigens. It is not present in all classes of antibody.

Antibodies are produced by B-lymphocytes.

To destroy pathogens within the body, either directly or by recruiting other immune cells.

• Anti-toxins

• Opsonins

• Agglutinins

Any three of:

• Pathogens and their toxins

• Pollen

• Blood cell surface molecules

• Surface proteins on transplanted tissues

A pathogen or virus may present multiple different antigens.

Each antigen has a different epitope, so a different specific antibody must be produced for each one.

False — the variable region, not the constant region, gives the antibody its specificity.

True — two heavy and two light chains held together by disulfide bonds.

An antibody that binds to a toxin produced by a pathogen (e.g. the bacteria causing diphtheria and tetanus), neutralising it and making it harmless.

An antibody that attaches to a pathogen (e.g. a bacterium) to make it more readily identifiable to phagocytes, promoting phagocytosis.

An antibody that causes pathogens carrying antigen-antibody complexes to clump together (agglutination).

The process in which antibodies attach to bacteria, marking them so that phagocytes can identify and engulf them more easily.

The clumping together of pathogens caused by agglutinin antibodies binding their antigens, reducing pathogen spread and allowing phagocytes to engulf many at once.

They bind to toxins produced by pathogens, which neutralises the toxins and makes them harmless.

They combine with the viruses and toxins, blocking them from entering or damaging the body's cells.

The phagocyte has receptor proteins for the heavy polypeptide chains of the antibodies.

Binding to these receptors enables phagocytosis to occur.

It makes the bacteria less mobile, which makes it easier for phagocytes to carry out phagocytosis.

• It reduces the chance that the pathogens will spread through the body

• It allows phagocytes to engulf a number of pathogens at one time

They create holes in the cell walls of the pathogen.

Water is then absorbed by osmosis, causing the pathogen to burst.

Antibodies that mark bacteria for easier recognition and engulfment by phagocytes are called opsonins.

Anti-toxins are antibodies that neutralise toxins produced by pathogens, making them harmless.

False — opsonins mark pathogens for phagocytosis; agglutinins cause clumping.

True

Immunity acquired when an antigen enters the body and triggers a specific immune response, in which the person's own body produces antibodies.

Immunity acquired without an immune response, in which antibodies are not produced by the person but are received ready-made from another source.

• Natural active immunity is acquired through exposure to microbes (an actual infection)

• Artificial active immunity is acquired through vaccination

In both natural and artificial active immunity the body produces memory cells (along with plasma cells), which remain in the body and give long-term immunity.

One to two weeks.

During the secondary response the antibody concentration in the blood:

• Increases over a much shorter period of time

• Reaches a higher concentration than after the first infection or vaccination

The person's immune system has not been activated, so no memory cells are produced. If the person is reinfected they would need another infusion of antibodies.

It is acquired by an injection / transfusion of ready-made antibodies.

For example, a person infected with tetanus is given an antitoxin (antibodies collected from people whose immune systems had been triggered by vaccination to produce tetanus antibodies).

• A foetus receives antibodies from the mother across the placenta

• A baby receives antibodies (the IgA isotype) in the first breast milk, the colostrum

There may not be enough time to actively acquire immunity, as producing antibodies via active immunity takes one to two weeks. Passive immunity provides ready-made antibodies immediately.

Babies receive antibodies in the first breast milk, known as the colostrum, which delivers the IgA isotype of antibody.

In active immunity the body produces the antibodies, whereas in passive immunity the body is given the antibodies.

False — passive immunity does not activate the immune system, so no memory cells are produced.

True

A condition in which the immune system damages the body's own cells because it recognises self-antigens as foreign.

An antigen found on the surface of an organism's own cells, which the immune system normally recognises as belonging to the body rather than as foreign.

The likelihood of an individual developing the disease when exposed to a specific pathogen or stimulus.

• Antibodies

• T cells (both helper and cytotoxic)

• B cells

These attack one or more self-antigens.

They act as surface antigens that enable the immune system to determine whether a cell belongs to the body or is foreign.

Both. The attack can be targeted at a single organ or directed at the entire body.

An autoimmune disease that solely affects the joints.

• Muscle spasms

• Inflamed tendons

• Lethargy

• Constant joint pain

• Genetics – susceptibility to an autoimmune disease can be inherited

• Environment – research suggests environmental factors are also important

When individuals moved from areas of low autoimmune disease prevalence (e.g. Japan) to areas of higher prevalence (e.g. the USA), they showed an increased chance of developing an autoimmune disease.

This suggests environmental factors, not just genetics, play a role.

In an autoimmune disease, antibodies, T cells and B cells attack one or more self-antigens found on the body's own cells.

Susceptibility to an autoimmune disease has been shown to be inherited, indicating that genetics is an influencing factor.

It usually begins in the fingers and hands, then spreads to the shoulders and elsewhere.

True

False — rheumatoid arthritis is an autoimmune disease of the joints, whereas osteoarthritis is a different, non-autoimmune condition.

A suspension of antigens intentionally put into the body to induce artificial active immunity — a specific immune response in which antibodies are released by plasma cells.

When a large proportion of the population has been vaccinated (and is therefore immune), making it difficult for a pathogen to spread. Those who are not immunised are protected because levels of the disease are so low.

When people living or working near a vulnerable (or infected) person are vaccinated to prevent them catching and transmitting the disease. The vaccinated individuals do not spread the pathogen, so vulnerable individuals "within the ring" are protected.

• Live attenuated vaccines

• Inactivated vaccines

They cause memory cells to be created.

When the antigen is re-encountered, the immune system produces antibodies in a faster, stronger secondary response.

• Contains whole pathogens that have been 'weakened'

• The weakened pathogens multiply slowly, allowing the body to recognise the antigens and trigger the primary immune response

• Tends to produce a stronger and longer-lasting immune response

• Can be unsuitable for people with weak immune systems, as the pathogen may divide before sufficient antibodies are produced (e.g. MMR)

• Contains whole pathogens that have been killed ('whole killed') or small subunit parts of the pathogen (e.g. proteins, sugars or toxoids)

• Cannot cause disease, so is safe even for those with weak immune systems

• Produces a weaker, shorter-lasting response, so repeated / booster doses are often required (e.g. polio, diphtheria)

Very few drugs are effective against viruses, so vaccines are one of the only reliable ways to control the spread of viral disease.

• People have a poor response (e.g. malnutrition or a defective immune system means they cannot produce enough antibodies)

• Antigenic variation — changes in pathogen antigens mean the vaccine no longer triggers an immune response; eukaryotic pathogens (e.g. malaria) have too many antigens

• Viruses can change their surface antigens (the targets of vaccines)

Antigenic drift — over time there are small changes in the structure and shape of the antigens (within the same strain of virus).

Antigenic shift — there are major changes in the antigens.

• Living inside cells

• Coating their bodies in host proteins

• Parasitising immune cells such as macrophages and T cells (e.g. HIV)

• Remaining in parts of the body that are difficult for vaccines to reach (e.g. Vibrio cholerae in the small intestine)

• Too few people in the community have been vaccinated

• Unstable political situations (e.g. civil unrest or war)

• Lack of public health facilities (poor infrastructure, few trained personnel, limited financial resources)

• The virus was stable — it did not mutate, so its surface antigens did not change and one vaccine could be used worldwide

• The live attenuated vaccine could be freeze-dried and stayed viable at high temperatures, suiting the tropics

• Symptoms made infected people easy to identify (surveillance was possible)

• Humans were the only reservoir and there were no carriers, making it easier to break the transmission pathway

The principles underpinning vaccination were discovered by Edward Jenner in the 1700s, when he developed the first smallpox vaccine.

True

False — live attenuated vaccines contain weakened whole pathogens; it is inactivated vaccines that contain killed pathogens.

Because there is a worrying increase in strains of antibiotic-resistant bacteria, meaning existing antibiotics are becoming less effective.

• Analysing 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 existing drugs using computer programmes that model molecular structures

• Identifying useful compounds produced by organisms (e.g. fungi, plants, animals and actinobacteria)

The genome can be analysed to find candidate genes that may code for potential drugs.

Bacteria and fungi.

They kill bacteria by inhibiting bacterial transcription.

Artemisinin is a drug found in Sweet wormwood that treats malaria.

Quinidine, derived from the Quinine tree, treats a fast heart rate.

Continued access to existing drugs and the discovery of new ones depends on the survival of species.

Microorganism and plant species may become extinct before we can discover what drugs they could provide.

The development of more targeted, personalised drugs to treat human diseases (as well as synthetic tissues), rather than a "one type fits all" approach.

The use of information about an individual's genes to influence their clinical care, for example prescribing the most effective drugs based on their genome.

Some individuals metabolise the drug slowly, making it an effective treatment.

Others metabolise it much faster, making it ineffective.

They can affect the tertiary structure of the proteins targeted by drugs, altering how effectively the drug works.

Herceptin is an antibody drug used to treat some breast cancers. A patient is only given the drug if they are found to have high numbers of a specific cell surface receptor.

It identifies individuals with a high chance of developing specific diseases, so that preventative measures can be taken.

It kills the pathogen while it is inside the red blood cells.

It blocks channel proteins in cardiac muscle to reduce impulse conduction.

False — rifamycins inhibit bacterial transcription, not translation.

True — this helps ensure individuals receive effective drugs with the least side effects.

A chemical substance that inhibits or kills bacterial cells with little or no harm to human tissue.

An antibiotic that kills bacteria.

An antibiotic that inhibits the growth processes of bacteria (rather than killing them directly).

An antibiotic that acts on a wide range of bacteria (e.g. amoxicillin).

An antibiotic that acts on a very small number of bacteria, used when a culture has shown which bacterium is causing the infection.

Antibiotics target prokaryotic features (structural or physiological) that are harmful to prokaryotic cells but usually do not affect eukaryotic (human) cells.

Penicillin was the first antibiotic to be discovered, in 1928, by Sir Alexander Fleming.

• Within a population there is genetic diversity; random mutation can produce an allele that confers resistance (not caused by antibiotic use)

• When an antibiotic is present, resistant individuals have a selective advantage and are more likely to survive and reproduce

• Non-resistant bacteria are more likely to die and not reproduce

• Resistance alleles are passed to offspring, so over several generations the whole population may become antibiotic-resistant

They have acquired genes coding for the enzyme β-lactamase (penicillinase), which breaks down penicillin.

Bacteria have a single loop of DNA with only one copy of each gene, so a new allele is not masked and is immediately displayed in the phenotype.

• Overuse of antibiotics / prescribing them when not necessary

• Large-scale use in farming to prevent disease, even when livestock are not sick

• Patients failing to complete the full course of antibiotics

• Only prescribe antibiotics when absolutely necessary and test the bacteria first

• Patients should finish the entire course even if they feel better

• Do not use antibiotics for viral infections

• Use narrow-spectrum rather than broad-spectrum antibiotics where possible

• Change the antibiotics prescribed so the same one is not always used

• Reduce and tightly control antibiotic use in agriculture

• Good hygiene practices such as handwashing and use of hand sanitisers

• Isolating infected patients to prevent spread, especially in surgical wards

Resistance alleles can pass between bacteria of different species on small circular pieces of DNA called plasmids, an example of horizontal gene transfer.

False — antibiotics have no effect on viruses; they only target bacteria.

True — surviving bacteria may include resistant individuals that then reproduce.