biology module 4 communicable diseases

infectious disease

disease caused by a pathogen that passes from infected individuals to uninfected individuals

non-infectious disease

Long-term diseases that are not caused by pathogens

bacteria

• 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

ring rot

• 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

viruses

• 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

tobacco mosaic virus

• 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

influenza

• 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

human immunodeficiency virus

• 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

protoctista malaria

Protists are unicellular eukaryotes

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

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

fungi

• 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

black sigatoka

• 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

what is disease transmission

• 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

transmission through spores

• pores 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

transmission of HIV

• 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

ways HIV can be transmitted

• 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

transmission of tuberculosis

• 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

transmission of malaria

• 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

what is transmission dependant on

• 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

passive defence mechanism

• 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

active defence mechanisms

• 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

waxy cuticle

• physical defence

  • 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

other examples of physical defences in plants

• Cellulose cell wall

• Closed stomata

• Bark

• Casparian strip

examples of chemical defences in plants

• 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

active defences

Hypersensitivity is the rapid death of tissue surrounding the infection site

• 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

salicylic acid

• 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

• 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)

first line of defence in humans

• The first line of defence prevents the entry of pathogens and is comprised of the following:

  • Skin

  • Mucous membranes

  • Expulsive reflexes

  • Chemical secretions

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

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

expulsive 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

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

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

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

  • Platelets release substances that undergo a series of chemical reactions 

  • The end product is that fibrin is formed, which forms a network, trapping platelets and forming a clot

• Blood clotting prevents excess blood loss, the entry of pathogens and provides a barrier (scab) for wound healing to occur

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

histamine

• 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

• 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

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

3 types of phagocyte

• Neutrophils

• Macrophages

• Dendritic cells

neutrophils

• Neutrophils are short-lived cells that 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

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

mode of action of neutrophil

• Chemicals released by pathogens, as well as chemicals released by the body cells under attack (e.g. 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 have antibodies attached to their surface antigens

  • 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

macrophage

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

• After being produced in the bone marrow, macrophages travel in the blood as monocytes, which then develop into macrophages once they leave the blood

  • After leaving the blood macrophages settle in the lungs, liver, spleen, kidney and lymph nodes

mode of action of neutrophil

• Macrophages play an important role in initiating the specific immune response

• They carry out phagocytosis in a similar way to neutrophils but they do not destroy pathogens completely; instead they cut the pathogens up so that they can display the antigens of the pathogens on their surface

  • Antigens are displayed as part of a structure called a major histocompatibility complex (MHC)

• The cell is now called an antigen-presenting cell and can be recognised by lymphocytes, another type of white blood cell

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

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

what is a blood smear

• 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

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

lymphocytes

• 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

what are the 2 types of lymphocytes

• T-lymphocytes (T cells)

  • Lymphocytes that mature in the thymus gland

• B-lymphocytes (B cells)

  • Lymphocytes that mature in the bone marrow

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 and T killer cells

process of T cells activation - antigen presentation

• Macrophages engulf pathogens and present the pathogen antigens on their own cell surface membrane

• They become antigen-presenting cells (APCs)

process of T cell activation - clonal 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

process of T cell activation - clonal 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

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

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

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

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

b cell activation - clonal selection and activation

• 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 cells

b cell activation - clonal expansion

• 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

primary immune response

(responding to a newly encountered antigen)

• 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

secondary immune response - b memory cells

• 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

secondary immune response - t memory cells

• 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

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

• 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

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

what is 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

how can antibodies act as anti toxins

• Antibodies can act as anti-toxins by binding to toxins produced by pathogens which neutralises them making them harmless

how can antibodies act as agglutins

• 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

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

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

• 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)

causes of autoimmune disease

• 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

effectiveness of vaccines

• 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

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)

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

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