Organisms that cause disease
Pathogen – a microorganism that causes disease
Transmission of Pathogens
Lifecycle of a pathogen:
- Travel from one host to another (transmission)
- Entering the hosts tissues
- Leaving the hosts tissues
Overcrowding, poor ventilation, poor health, poor diets, homelessness and living and working with people who have migrated from areas where disease is more common, all may affect the likelihood of catching a disease.
Some pathogens, like the protoctista plasmodium that causes malaria, use vectors for transmission.
Indirect transmission of plant pathogen occurs as a result of insect attack.
The fungus that causes Dutch elm disease is carried by the beetle Scolytus multistriatus
Plant Defences against pathogens
- Physical Defences
- Cellulose cell wall – this acts as a physical barrier but also contains many chemical defences that can be activated when a pathogen is detected
- Thickening of the cell wall with lignin – lignin is a phenolic compound and completely waterproof as well as largely indigestible
- Waxy cuticles – these prevent water collecting on the cell surfaces which removes the water that the pathogenic cells need to survive
- Bark – most back also contains a variety of chemical defences as well as being a physical barrier to disease
- Stomatal closure- stomata are possible points of entry for pathogens and so the guard cells can close them when pathogenic organisms are detected
- Callose – callose is a large polysaccharide that is deposited in the sieve tubes at the end of the growing season around the sieve plates and blocks the flow in the tube. This can prevent a pathogen spreading around the plant
- Tylose formation – tylose is a balloon like swelling or projection that fills the xylem vessel, when fully formed it can completely block off that part of the xylem vessel. It also contains a high concentration of chemicals such as terpenes that are toxic to pathogens
- Chemical Defences
- Plant tissues contain a variety of chemicals that have anti-pathogenic properties including terpenoids, phenols, alkaloids and hydrolytic enzymes.
- Some of these chemicals such as the terpenes in tyloses and the tannins in bark are present before infection. However, because the production of chemicals requires a lot of energy, many chemicals are not produce until after an infection is discovered.
- Cell walls become thickened and strengthened with additional cellulose
- Deposition of callose between the plant cell wall and cell membrane near the pathogen. Callose deposits impeded cellular penetration at site of infection, strengthen the cell wall and block of plasmodesmata.
- Oxidative bursts that produce highly reactive oxygen molecules capable of damaging the cells of invading pathogens
- An increase in the production of chemicals
- Necrosis – deliberate cell suicide
- Canker – a sunken necrotic lesion in the woody tissue such as the main stem or branch that causes the death of the cambium tissue in the bark.
Primary Defences against Disease
Primary defences are the defences in place that prevent pathogenic material from entering the body.
The skin is the main primary defence. The outer layer of skin is called the epidermis and consists of layers of keratinocytes. The keratinocytes are produces at the base of the epidermis and migrate out to the surface of the skin, slowly drying out and their cytoplasm in replaced by the protein keratin in the process of keratinisation. By the time the cells reach the surface they are dead. The layer of dead keratinised cells act as effective layer of disease prevention.
Blood Clotting and skin repair
- Abrasions or lacerations damage the skin and open the body to infection
- The body prevents excess blood loss by forming a clot and making a temporary seal to prevent infection
- Calcium ions and 12 clotting factors are released from the platelets and damaged tissue
- Damage to blood vessel exposes collagen
- Platelets bind to collagen fibres and release clotting factors, a temporary plug is formed
- Inactive thrombokinase in blood (factor X) is turned into active thrombokinase (an enzyme)
- Prothrombin in blood and thrombonkinase and Ca2+ ions make active thrombin
- Active thrombin turns the soluble fibrinogen in the plasma into insoluble fibrin which attach to the platelets in the plug and clot, trapping more red blood cells and platelets.
- As the skin grows and the scab shrinks the edges of the laceration are pulled together.
The epithelial layer contains mucus-secreting cells called goblet cells and also mucus secreting glands under the epithelium.
The mucus traps any pathogens that may be in the air
The epithelium is also ciliated
Cilia are tiny hair-like organelles that can move in a coordinated fashion to waft the mucus along.
Coughing and sneezing – areas that are prone to microorganism attack are sensitive and respond to irritations by coughing sneezing and vomiting in the hope that the expulsion of air will propel the pathogen from the body.
Inflamation – the tissue may be hot and painful as the presence of harmful microorganisms has been detected by mast cells which release a cell signalling substance called histamine which causes vasodilation to make the capillary walls more permeable to white blood cells and proteins. The increased production of tissue fluid causes the swelling (oedema)
Eyes are protected by antibodies and enzymes in tear fluid
The ear canal is lined with wax
The female reproductive system is protected by a mucus plug in the cervix and by maintaining relatively acidic conditions in the vagina.
Specific Immune Response
Antibodies – specific proteins released by plasma cells that can attach to pathogenic antigens
Clonal expansion – an increase in the number of cells by mitotic cell division
Interleukins – signalling molecules that are used to communicate
Specific immune response involves B lymphocytes (B cells) and T lymphocytes (T cells) which are white blood cells with specialised receptors on their cell surface membranes. Antibodies are produced by B lymphocytes, and these neutralise foreign antigens. Long term disease protection is provided. An immunological memory is produced as B memory cells are released and circulate in the body for a number of years.
- Pathogen enters the body
- The antigens on the pathogen are presented on the pathogens cell membrane as it travels in the body fluids, on infected cells, and on the plasma membrane of macrophages that have engulfed the pathogens during the secondary non-specific response.
- T cells (from thymus) and B cells (from bone marrow) must detect the antigen from one of these three sources
- The detection of the pathogenic antibodies triggers clonal expansion in both T and B cells.
- T helper cells release cytokines that further stimulate the development of B cells
- Proliferation occurs once the correct lymphocytes have been activated.
- Cells differentiate and T & B memory cells are produced to remain in the blood should the body ever come under attack from the same pathogen again.
- T killer cells attack infected host cells and plasma cells make antibodies (the differentiation for this is triggered by cytokines from the macrophages
- Finally T regulator cells end the immune response to prevent the attack of the body’s own cells.
Come from the bone marrow and develop in the thymus
T helper cells (Th) – release cell signalling molecules (cytokines) that stimulate the immune response of B cells to develop and stimulate phagocytosis by phagocytes
T killer cells (Tk) – attack and kill host-body cells that display the foreign antigen as well as infected body cells
T memory cells (Tm) – provide long term immunity by staying in the blood for a long time
T regulator cells (Tr) – inhibit and end the immune response, preventing autoimmunity
They are involved in cell-mediated response (combat microorganisms)
They are a complementary shape to the antigen of pathogens and once the T cell has found a complementary antigen clonal expansion takes place produced by mitosis
Grow completely in the bond marrow
Plasma cells – derived from the B lymphocytes, these cells manufacture antibodies
B memory cells – cells that remain in the blood for a long time, providing long-term immunity
They are involved in the humoral response (producing antibodies)
Macrophages release monokines which attract neutrophils (by chemotaxis – the movement of cells towards a particular chemical) and stimulate differentiation of B cells (and the release of antibodies)
T cells and macrophages release interleukins which stimulate clonal expansion (proliferation) and the differentiation of B & T cells
Many cells release interferon which inhibits virus replication and stimulates T killer cells
A disease that occurs when the immune system attacks a part of the body
Arthritis – a painful inflammation of a joint that starts with antibodies attacking the membranes around the joint
Lupus – swelling and pain in any part of the body, antibodies attack certain proteins in the nucleus of cells and affected tissue
Antigens are molecules that stimulate an immune response, usually proteins/glycoproteins in the pathogen’s plasma membrane, and when detected the production of antibodies is commenced.
Antibodies are specific to the antigen as antigens are specific to the organism. Our own antigens are recognised as ‘self’ by the immune system and do not provoke a response
Antibodies are immunoglobins (complex proteins produces by the plasma cells) and are released in response to an infection, they have a region with a specific shape to the antigen, antibodies attach to antigens and render them harmless
4x polypeptide chain, 2x light chains & 2x heavy chains
The tips of the y are the variable region but is the same for every type of antibody
A group of antibodies that bind to pathogen antigens and then act as binding sites for phagocytic cells
Some are non-specific
Some are produced as part of a specific immune response and bind to specific antigens
Antibodies flag up a pathogen for the phagocyte/attach to antigen which has a use to the pathogen, disabling it.
They also prevent the pathogen to enter the host cell.
Neutralise pathogens that use their antigens to bind to host cells etc.
By attaching onto the pathogen they make them easier to identify and easier for the phagocytes to bind to them/engluf them.
Antibodies that cause the pathogens to stick together (agglutinate) by making crosslinks between their antigens
This makes the pathogen non-effective and easily phagocytosed
Some antibodies bind to molecules that are release by pathogenic cells. These molecules may be toxic and the action of anti-toxins render them harmless.
Primary and Secondary Responses
Primary immune response – initial response caused by a first infection
Secondary immune response – more rapid and vigorous response caused by a second or subsequent infection by the same pathogen
- infection by pathogen
- lag phase
- antibodies produced
- antibody level rises to combat infections
- pathogen dealt with
- antibody level declines – short lived
- secondary immune response is much faster
Vaccination – a way of stimulating an immune response so that immunity is achieved, provides immunity to specific disease by deliberate exposure to a weakened/dead strain of antigenic material
Antigenic material takes many forms:
- Whole live microorganisms (usually not very harmful g. smallpox which prevents cowpox virus, a much nastier disease)
- Harmless attenuated version of the pathogenic organism e.g. measles & TB
- Dead pathogen e.g. typhoid
- Antigen preparations only, no actual pathogen e.g. hep B
- Toxoids – harmless version of a toxin e.g. tetanus
- Herd vaccination – providing the vaccine to all or almost all of the population so that the pathogen cannot spread, it is necessary to vaccinate 80 – 95% of the population to completely immunise the population
- In the UK young children are immunised against the following diseases: diphtheria, tetanus, whooping cough, polio, meningitis, measles, mumps and rubella.
- Ring vaccination – used when a new disease case is reported, vaccinated all people in the immediate vicinity of the case, also used to control livestock disease
- Epidemic – a rapid spread of disease through a high proportion of the population
- Influenza – a killer disease caused by a virus, people aged 65+ are most at risk as well as people with respiratory tract problems, the swine flu pandemic is an example of this virus
Types of immunity
Active immunity – immune system activated and own antibodies manufactured
Artificial immunity – immunity achieved as a result of medical intervention
Natural immunity – immunity achieved through normal life processes
Passive immunity – immunity achieved when antibodies are passed to the individual through breast feeding or injection
Development of Drugs
Antibiotic – a chemical which prevents the growth of microorganisms, can be antibacterial or antifungal
Personalised medicine – development of designer medicines for individuals
Synthetic biology – re-engineering of biology, from the production of new molecules that mimic a natural process to the use of natural molecules to produce new biological systems that do not exist in nature
The antibiotic penicillin was discovered by Alexander Fleming accidentally.
Morphine originated in the use of sap from unripe poppy seed heads in Neolithic times, in the 12th century the opium from poppies was used as an anaesthetic and by the 19th century morphine and opium were used to reduce nervous action in the central nervous system
Willow bark is used to relieve pain and fever. Its active ingredient was found to reduce the side effect of stomach bleeding by adding an acetyl group which lead to the development of aspirin and ibuprofen
Monkeys, bears and other animals rub citrus oils on their coats as insecticides and antiseptics to prevent insect bites and infection. Birds line their nests with medicinal leaves to protect young from blood sucking mites. Chimps swallow leaves folded in a particular way to remove parasites from the digestive tract
Further plant research
Scientists use the traditional plant medicines as a starting point for new medicines and then try to isolate their active ingredient.
Pharmaceutical companies also research the way that microorganisms cause disease so that they can model ideal proteins and glycoproteins to act as medicines on these drugs. E.g. the HIV virus binds to the CD4 and CCR5 receptors on T helper cells. In order to cure this scientists are experimenting with blocking this binding with other similarly shaped proteins generated in computer models.
Overuse and misuse of antibiotics have enabled microorganisms to develop resistance which limits the effectiveness of current medicines.