6.3 Defence Against Infectious Diseases Flashcards
Pathogen
is a disease causing agent that disrupts the normal physiology of the infected organism
Bacteria
Bacteria are unicellular prokaryotic cells that can reproduce quickly and compete with host cells for space and nutrition
Most bacteria are relatively harmless and some may even form mutualistic relationships with hosts (e.g. normal gut flora)
Bacteria may cause disease by producing toxic compounds (exotoxins) or releasing the substances when destroyed (endotoxins)
As the toxins retain their destructive capacity beyond bacterial death, they are often the cause of food poisoning
Reproduce by binary fission
Viruses
Viruses are metabolically inert and incapable of reproducing independently of a host cell (hence are non-living)
They typically consist of an inner core of nucleic acid surrounded by a protein coat (capsid)
Simpler viruses may lack a capsid (viroids), whilst more complex viruses may possess an external lipid envelope
Viruses can be either DNA-based (adenoviruses) or RNA-based (retroviruses)
Virus reproduction
The virus attaches itself to the host cell by its tail, an injects its own genetic material into the cell, leaving the protein coat on the outside
The virus RNA invades the cell nucleus and takes over
Viral RNA uses the host cell to create new RNA and assemble more viral parts
New viral particles are released, sometimes destroying the cell in the process
Symptoms
is a response of the body to the disease which can be observed
It may be due to the pathogen damaging cells or it may be due to the immune system’s response
How infectious diseases are spread
passed from one individual to another:
- by direct contact (e.g STDs)
- by insect bites (e.g. malaria)
- through the air by coughing and sneezing
- by contaminated food and water (e.g. cholera)
may enter the body:
- through natural openings
- through untreated wounds
- through bites from insects
First line of defence
The primary defence against infectious disease are the surface barriers that prevent pathogens from entering the body
These surface barriers include intact skin (protect external boundaries) and mucous membranes (protect internal boundaries)
Both the skin and mucous membranes release chemical secretions which restrict the growth of microbes on their surfaces
If pathogens cannot enter the host body, they cannot disrupt normal physiological functions and cause disease
Second line of defence
The second line of defence against infection are the non-specific cellular and molecular responses of the innate immune system
These defences do not differentiate between different types of pathogen and respond the same way upon every infection
Phagocytic leukocytes migrate to infection sites and engulf foreign bodies (dendritic cells then present antigens to lymphocytes)
Inflammatory responses increase capillary permeability at infected sites, recruiting leukocytes but leading to localised swelling
Antimicrobial proteins (such as cytokines and complement proteins) regulate immune activity within the body
Fever increases body temperatures to activate heat-shock proteins and suppress microbial growth and propagation
Third line of defence
The final line of defence against infection are the lymphocytes that produce antibodies to specific antigenic fragments
Each B cell produces a specific antibody, and the body has millions of different B cells capable of detecting distinct antigens
Helper T cells regulate B cell activation, ensuring that antibodies are only mass-produced at the appropriate times
Both B and T cells will differentiate to form memory cells after activation, conferring long-term immunity to a particular pathogen
Surface barriers
skin - waterproof, tough layers of epidermal cells that are frequently replaced
sebum - secreted by oil glands (antimicrobial)
earwax - secreted by skin lining the outer ear
sweat - salty secretions
tears - salty antiseptic and contain lysozyme enzyme that destroys bacteria
mucus (mouth, nose, lungs, vagina and anus), sticky secretion that traps pathogens and dust. Wave like motion of cilia hairs that line the trachea and bronchi sweep mucus and trapped pathogens out of respiratory systems
stomach acid
Blood clots
Clotting (haemostasis) is the mechanism by which broken blood vessels are repaired when damaged
Clotting functions to prevent blood loss from the body and limit pathogenic access to the bloodstream when the skin is broken
There are two key components of a blood clot – platelets and insoluble fibrin strands
Platelets undergo a structural change when activated to form a sticky plug at the damaged region (primary haemostasis)
Fibrin strands form an insoluble mesh of fibres that trap blood cells at the site of damage (secondary haemostasis)
Coagulation cascade
The process by which blood clots are formed involves a complex set of reactions collectively called the coagulation cascade
This cascade is stimulated by clotting factors released from damaged cells (extrinsic pathway) and platelets (intrinsic pathway)
The coagulation cascade involves many intermediary steps, however the principal events are as follows:
Clotting factors cause platelets to become sticky and adhere to the damaged region to form a solid plug
These factors also initiate localised vasoconstriction to reduce blood flow through the damaged region
Additionally, clotting factors trigger the conversion of the inactive zymogen prothrombin into the activated enzyme thrombin
Thrombin in turn catalyses the conversion of the soluble plasma protein fibrinogen into an insoluble fibrous form called fibrin
The fibrin strands form a mesh of fibres around the platelet plug and traps blood cells to form a temporary clot
When the damaged region is completely repaired, an enzyme (plasmin) is activated to dissolve the clot
Coronary heart disease
Coronary thrombosis is the formation of a clot within the blood vessels that supply and sustain the heart tissue (coronary arteries)
Occlusion of a coronary artery by a blood clot may lead to an acute myocardial infarction (heart attack)
Blood clots form in coronary arteries when the vessels are damaged as a result of the deposition of cholesterol (atherosclerosis)
Atheromas (fatty deposits) develop in the arteries and significantly reduce the diameter of the lumen (stenosis)
The restricted blood flow increases pressure in the artery, leading to damage to the arterial wall (from shear stress)
The damaged region is repaired with fibrous tissue which significantly reduces the elasticity of the vessel wall
As the smooth lining of the artery is progressively degraded, lesions form called atherosclerotic plaques
If the plaque ruptures, blood clotting is triggered, forming a thrombus that restricts blood flow
If the thrombus is dislodged it becomes an embolus and can cause a blockage in a smaller arteriole
Antigen
general term for any foreign organism or toxin inside the body
it is recognised by the body as foreign by unique proteins that all cells have on their surface
Leucocytes
general term for white blood cells
bone marrow is where they are produced
two types: phagocytes and lymphocytes
Innate immune system
It does not differentiate between different types of pathogens (non-specific)
It responds to an infection the same way every time (non-adaptive)
Phagocytes
Phagocytosis is the process by which solid materials (such as pathogens) are ingested by a cell (i.e. cell ‘eating’ via endocytosis)
Phagocytic leukocytes circulate in the blood and move into the body tissue (extravasation) in response to infection
Damaged tissues release chemicals (e.g. histamine) which draw white blood cells to the site of infection (via chemotaxis)
Pathogens are engulfed when cellular extensions (pseudopodia) surround the pathogen and then fuse to form an internal vesicle
The vesicle is then fused to a lysosome (forming a phagolysosome) and the pathogen is digested
Pathogen fragments (antigens) may be presented on the surface of the phagocyte in order to stimulate the third line of defence
Macrophages
special phagocytes that engulf antigens, process them, then attach them to membrane proteins and are displayed on the surface of the macrophage
These then present them to the T-lymphocytes which stimulate B lymphocytes to make antibodies