6.3 Defence Against Infectious Diseases Flashcards

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1
Q

Pathogen

A

is a disease causing agent that disrupts the normal physiology of the infected organism

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2
Q

Bacteria

A

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

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3
Q

Viruses

A

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)

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4
Q

Virus reproduction

A

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

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5
Q

Symptoms

A

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

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6
Q

How infectious diseases are spread

A

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

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7
Q

First line of defence

A

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

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8
Q

Second line of defence

A

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

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9
Q

Third line of defence

A

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

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10
Q

Surface barriers

A

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

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11
Q

Blood clots

A

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)

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12
Q

Coagulation cascade

A

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

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13
Q

Coronary heart disease

A

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

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14
Q

Antigen

A

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

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15
Q

Leucocytes

A

general term for white blood cells
bone marrow is where they are produced
two types: phagocytes and lymphocytes

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16
Q

Innate immune system

A

It does not differentiate between different types of pathogens (non-specific)
It responds to an infection the same way every time (non-adaptive)

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17
Q

Phagocytes

A

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

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18
Q

Macrophages

A

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

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19
Q

Neutrophils

A

most common phagocyte, rapidly engulf invaders
do not return to the blood, turn to pus and die

20
Q

Inflammation

A

enables the cells of the immune system to be rapidly brought to the affected area by the blood
causes redness, swelling, heat and pain
these are due to histamine which is released by white blood cells at the injured site

21
Q

Histamine effects

A

widens blood vessels (vasodilation) especially in the arterioles, which increases the blood flow to the area and thus supply defence cells
makes capillaries more ‘leaky’ enabling antibodies to escape into the surrounding tissues

22
Q

Adaptive immune system

A

It can differentiate between particular pathogens and target a response that is specific to a given pathogen
It can respond rapidly upon re-exposure to a specific pathogen, preventing symptoms from developing (immunological memory)

23
Q

Lymphocytes

A

B lymphocytes (B cells) are antibody-producing cells that recognise and target a particular pathogen fragment (antigen)
Helper T lymphocytes (TH cells) are regulator cells that release chemicals (cytokines) to activate specific B lymphocytes

When phagocytic leukocytes engulf a pathogen, some will present the digested fragments (antigens) on their surface

These antigen-presenting cells (dendritic cells) migrate to the lymph nodes and activate specific helper T lymphocytes
The helper T cells then release cytokines to activate the particular B cell capable of producing antibodies specific to the antigen
The activated B cell will divide and differentiate to form short-lived plasma cells that produce high amounts of specific antibody
Antibodies will target their specific antigen, enhancing the capacity of the immune system to recognise and destroy the pathogen
A small proportion of activated B cell (and activated TH cell) will develop into memory cells to provide long-lasting immunity

24
Q

Antibodies

A

is a protein produced by B lymphocytes (and plasma cells) that is specific to a given antigen
the antibodies combine with the antigens causing them to lump together making them easier to be destroyed by phagocytes or they may lock onto the antigen and destroy it

25
Q

Structure of antibodies

A

Antibodies are made of 4 polypeptide chains that are joined together by disulphide bonds to form Y-shaped molecules
The ends of the arms are where the antigen binds – these areas are called the variable regions and differ between antibodies
The rest of the molecule is constant across all antibodies and serves as a recognition site for the immune system (opsonisation)

26
Q

HIV

A

The Human Immunodeficiency Virus (HIV) is a retrovirus that infects helper T cells, disabling the body’s adaptive immune system

It causes a variety of symptoms and infections collectively classed as Acquired Immuno-Deficiency Syndrome (AIDS)

27
Q

Effects of HIV

A

HIV specifically targets the helper T lymphocytes which regulate the adaptive immune system
Following infection, the virus undergoes a period of inactivity (clinical latency) during which infected helper T cells reproduce
Eventually, the virus becomes active again and begins to spread, destroying the T lymphocytes in the process (lysogenic cycle)
With a reduction in the number of helper T cells, antibodies are unable to be produced, resulting in a lowered immunity
The body becomes susceptible to opportunistic infections, eventually resulting in death if the condition is not managed

28
Q

Transmission of HIV

A

HIV is transmitted through the exchange of body fluids (including unprotected sex, blood transfusions, breastfeeding, etc.)
The risk of exposure to HIV through sexual contact can be minimised by using latex protection (i.e. condoms)
A small minority of people are immune to HIV infection (they lack the CD4+ receptor on TH cells that HIV requires for docking)
HIV is a global issue, but is particularly prevalent in poorer nations with poor education and health systems

29
Q

Social implications of HIV/AIDS

A

families and friends suffer grief
families become poorer if the individual with AIDS was the wage earner is refused life insurance
individuals infected with HIV may become stigmatized and not find partners
sexual activity in a population may be reduced because of the fear of AIDS

30
Q

Immunity

A

is the ability of an organism to resist disease

31
Q

Natural immunity

A
  1. the person has had the disease and has made their own antibodies. This immunity lasts a long time. (Active natural immunity)
  2. in babies when antibodies pass from the mother across the placenta. This immunity is short term but gives the baby protection for the first fe weeks. (passive natural immunity)
32
Q

Artificial immunity

A
  1. The person is injected with ready made antibodies. The advantage is that the person gains immediate immunity and can provide a cure for a person who is already infected, but the immunity is only short term because the person has not made the antibodies. (Passive artificial immunity)
  2. when a person’s immune system is stimulated to make antibodies. Often a small amount of fluid containing dead bacteria or viruses is injected into blood. Your body then produces antibodies to fight this particular disease. Immunity generally lasts a long time. (Active artificial immunity)
33
Q

Principle of vaccination

A

antigens in the vaccine cause the production of the antibodies needed to control the disease.
induce long-term immunity to specific pathogenic infections by stimulating the production of memory cells

34
Q

Live attenuated vaccines

A

contains bacteria or viruses that have been weakened so that they cannot cause disease. Stimulate a immune response.

35
Q

Dead (inactivated) vaccines

A

contain bacteria or viruses that have been killed or inactivated. With inactivated vaccines, you usually need many doses to give full protection against diseases.

36
Q

Subunit vaccines

A

contain parts of bacteria or viruses or bacterial toxins that have been made harmless

37
Q

Nucleic acid (RNA) vaccines

A

adding a small amount of the virus genetic code into the body stimulate an immune response

38
Q

Herd Immunity

A

is when individuals who are not immune to a pathogen are protected from exposure by the large amounts of immune individuals within the community

39
Q

Antibiotics

A

Antibiotics are compounds that kill or inhibit the growth of microbes (specifically bacteria) by targeting prokaryotic metabolism

Metabolic features that may be targeted by antibiotics include key enzymes, 70S ribosomes and components of the cell wall
Because eukaryotic cells do not possess these features, antibiotics will target the pathogenic bacteria and not the infected host
Antibiotics may either kill the invading bacteria (bactericidal) or suppress its potential to reproduce (bacteriostatic)

40
Q

Antibiotics and viruses

A

Viruses do not possess a metabolism (they are not alive) and instead take over the cellular machinery of infected host cells

As such, they cannot be treated with antibiotics and must instead be treated with specific antiviral agents
Antiviral treatments target features specific to viruses (e.g. viral enzymes like reverse transcriptase or components of the capsid)

41
Q

Penicillin - Flemming

A

The first chemical compound found to have antibiotic properties was penicillin, which was identified by Alexander Fleming in 1928

The discovery of penicillin was a fortuitous accident, resulting from the unintended contamination of a dish containing S. aureus
A Penicillium mould began to grow on the plate and a halo of inhibited bacterial growth was observed around the mould
Fleming concluded that the mould was releasing a substance (penicillin) that was killing the nearby bacteria

42
Q

Florey and Chain

A

tested penicillin on infected mice
Eight mice were injected with hemolytic streptococci and four of these mice were subsequently injected with doses of penicillin
The untreated mice died of bacterial infection while those treated with penicillin all survived – demonstrating its antibiotic potential

43
Q

Antibiotic resistance

A

Some strains of bacteria have evolved with genes that confer resistance to antibiotics and some strains have multiple resistance

Genes may confer resistance by encoding traits that degrade the antibiotic, block its entry, increase its removal or alter the target
Because bacteria reproduce at a rapid rate, resistant strains of bacteria can proliferate very quickly following the initial mutation
Additionally, resistant strains can pass resistance genes to susceptible strains via bacterial conjugation (horizontal gene transfer)

The prevalance of resistant bacterial strains is increasing rapidly with human populations due to a number of factors:

Antibiotics are often over-prescribed (particularly broad-spectrum drugs) or misused (e.g. given to treat a viral infection)
Many antibiotics are freely available without a prescription and certain antibiotics are commonly included in livestock feed
Multi-drug resistant bacteria are especially common in hospitals (i.e. nosocomial infections) where antibiotic use is high

An example of an antibiotic resistant strain of bacteria is Golden Staph (MRSA – Methicillin Resistant Staphylococcus aureus)

44
Q

Monoclonal antibodies

A

Monoclonal antibodies are antibodies artificially derived from a single B cell clone (i.e. identical specific antibodies)

An animal (typically a mouse) is injected with an antigen and produces antigen-specific plasma cells
The plasma cells are removed and fused (hybridised) with tumor cells capable of endless divisions (immortal cell line)
The resulting hybridoma cell is capable of synthesising large quantities of monoclonal antibody

45
Q

Treatment use of monoclonal antibodies

A

Monoclonal antibodies are commonly used to provide immune protection for individuals who contract harmful diseases

Because the rabies virus can potentially be fatal, injecting purified antibodies functions as an effective emergency treatment
Monoclonal antibodies can be used to target cancer cells that the body’s own immune cells fail to recognise as harmful

46
Q

Diagnostic use of monoclonal antibodies - pregnancy tests

A

Pregnancy tests use a process called ELISA (enzyme-linked immunosorbent assay) to identify a substance via a colour change

Free monoclonal antibodies specific to hCG are conjugated to an enzyme that changes the colour of a dye
A second set of monoclonal antibodies specific to hCG are immobilised to the dye substrate
If hCG is present in urine, it will interact with both sets of monoclonal antibody (forming an antibody ‘sandwich’)
When both sets of antibody are bound to hCG, the enzyme is brought into physicial proximity with the dye, changing its colour
A third set of monoclonal antibodies will bind any unattached enzyme-linked antibodies, functioning as a control

47
Q

Clonal selection

A

Mitotic division of B cells activated in response to an infection