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Communicable Disease Flashcards

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1
Q

What are communicable diseases?

A
  • Can be spread between organisms of the same species or sometimes between different species.
  • Spready by PATHOGENS
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2
Q

What are PATHOGENS?

A

microorganisms which can causes disease.

  • HOST ~ the organism which the pathogen infects

FOUR main categories:
- bacteria
- virus
- fungi
- protoctista / protista

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3
Q

Bacteria

A
  • PROKARYOTIC cells
  • Once they enter the body, release TOXINS.
  • Toxins ~ chemicals which damage host cells and tissues leading to symptoms of the disease
  • Divide rapidly by BINARY FISSION
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4
Q

Examples of Bacterial diseases

A

TUBERCULOSIS:
- affects many part of the body , mostly the LUNGS
- kills the cells and tissues

MENINGITIS:
- infection of the MENINGES ~ the membrane that surround the brain & spinal cord
- The membranes become swollen and may cause damage to the brain & nerves

RING ROT ( plants):
- Ring of decay in the VASCULAR TISSUE
- infect potato tuber and tomato
- Cause leaf wiltering

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5
Q

Viruses

A
  • Much SMALLER than bacteria
  • NON-LIVING
  • Have no cellular structure
  • PREVENT a host cell from functioning normally and can lead to the death of the host cell
  • Consist of GENETIC MATERIAL which can be DNA or RNA which is wrapped in a protein structure , CAPSID.
  • ATTACHMENT PROTEINS ~ allow the virus to attach to host cells
  • Some contain a LIPID MOLECULE
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6
Q

How do viruses REPRODUCE?

A
  • CANNOT reproduce OUTISIDE of a host cell

To reproduce:

  • a virus ATTACHES to the host cell and then passes through the CELL MEMBRANE
  • COPIES itself using the ENZYMES of the host cell
  • Virus particles now LEAVE the host cell and can go on to infect NEW host cells and continue REPRODUCING
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7
Q

Examples of VIRUSES

A

HIV/AIDS:
- attacks T helper cells , preventing
immune system from working effectively
- Leads to AIDS ~ causes opportunistic
infections , e.g tuberculosis
- caused by infected needles

INFLUENZA (flu):
- Attacks respiratory system
- causes muscle pain & headaches

TOBACCO MOSAIC VIRUS (plants):
- causes mottling & decolouration of leaves

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8
Q

Fungi

A
  • EUKARYOTIC organisms
  • Can be UNICELLULAR or MULTICELLULAR
  • Obtain NUTRIENTS by releasing enzymes and DIGESTING the material around them
  • The PRODUCTS of digestion are then absorbed back into the fungal cells
  • Causes DAMAGE to host cells & tissues
  • SPORES ~ released when they reproduce and cause fungal diseases to spread very WIDELY
  • Some found in REMAINS of dead bodies where they take part in the DECAY process
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9
Q

Examples of fungal infections

A

BLACK SIGATOKA :
- infects plants, mainly BANANAS
- causes leaf spots which reduce yields

RINGWORM:
- infects CATTLE
- growth of fungus in skin withs spore cases erupting through skin to cause a RASH

ATHLETES FOOT:
- growth under skin of feet
- Particularly between the toes

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10
Q

Examples of PROTISTA diseases

A

BLIGHT:
- Affects tomatoes & potatoes
- causes damage to potato tubers & leaves

MALARIA:
- parasite in the blood
- causes headaches and fever
- can progress to coma and death
- caused by PLASMODIUM

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11
Q

Protocista/ protista

A
  • EUKARYOTIC organisms
  • Cause harm by entering host cells and feeding on their contents as they grow
  • GIARDIA ~ causes diarrhoea and is transmitted when humans drink water containing infected faeces
  • PLASMODIUM ~ causes malaria in humans and is transmitted between humans by mosquitos
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12
Q

Direct transmission and factors that affect these

A

Direct physical contact :
- hygiene
- e.g washing hands regularly
- cleaning surfaces

Faecal ( contamination of food and drink):
- Washing all fresh food
- Treatment of waste water
- thorough cooking of all food

Droplet infection:
- cover mouth when sneezing or coughing
- using a tissue then disposing correctly

Spores:
- washing skin after contact with soil
- use of a mask

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13
Q

SOCIAL FACTORS that affect transmission

A

OVERCROWDING:
- Many people living and sleeping together in one house

POOR VENTILATION

POOR HEALTH:
- Particularly those with HIV/AIDS, as they are more likely to contract more diseases

POOR DIET

HOMELESSNESS

MIGRATION :
- Living or working with people who have migrated from areas where a disease is more common

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14
Q

Indirect transmission

A

Passing a pathogen from host to new host via a VECTOR.

VECTOR ~ an organism that carries a pathogen from one host to another

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15
Q

PASSIVE DEFENCES of plants against pathogens

A

These are present BEFORE infection and their role is to PREVENT ENTRY & SPREAD of the pathogen:

CELLULOSE CELL WALL ~ acts as a physical barrier but also can have a variety of chemicals that are activated

LIGNIN THICKENING :
- Prevent water form collecting on the cell surfaces
- pathogens need water to survive

BARK:
- contains chemical defences such as TENNINS

STOMATAL CLOSURE :
- Controlled by guard cells
- when pathogen is detected guard cells close stomata

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16
Q

Callose & Tylose formation

A

Types of chemical & passive defence against pathogen in PLANTS:

CALLOSE ~ phloem
- Large polysaccharide
- deposited around the sieve plates
- BLOCKS the flow in the sieve tube
- prevents pathogen from spreading around the plant

TYLOSE ~ xylem
- Balloon-like swelling or projection
- plugs the vessel so it can no longer carry water
- BLOCKS XYLEM vessels
- contains TERPENES which is TOXIC to pathogens

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17
Q

ACTIVE defences of plants against pathogens

A

When a pathogen attacks, the plant responds by fortifying the defences already present:

ADDITIONAL CELLULOSE:
- Cell wall becomes thickened and strengthened

DEPOSITION OF CALLOSE:
Between the plant cell wall and cell membrane near the invading pathogen

OXIDATIVE BURSTS:
- Produce highly reactive oxygen molecules capable of damaging the cells of invading organisms

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18
Q

CHEMICAL defences of plants against pathogens

A

TERPENOIDS:
- Essential oils with antibacterial & antifungal properties
- Can create SCENT e.g menthols by mint plants

PHENOLS:
- Antibiotic & antifungal properties
- TANNINS found in bark inhibit attack by insects
- DEACTIVATE salivary proteins & digestive enzymes causing death

ALKALOIDS:
- Nitrogen-containing ~ caffeine, nicotine, cocaine
- Give a BITTER taste
- Inhibit enzymes involve in metabolic reactions e.g protein synthesis

DEFENSINS:
- Small cysteine-rich proteins
- Have broad anti -microbial activity
- Work in plasma membrane of pathogen, inhibiting the action of ion transport channels

HYDROLYTIC ENZYMES:
- Found in spaces between cells
- CHITINASES ~ breaks down chitin in fungal cell walls
- GLUCANASES ~ hydrolyse glycosidic bonds in glucans
- LYSOZYMES ~ degrade bacterial cells walls

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19
Q

Necrosis & Canker

A

PLANT defences against pathogens that cause DEATH of a part of the plant:

NECROSIS:
- Deliberate cell suicide
- some cells are sacrificed to save the rest of the plant
- Limits the pathogens access to water an nutrients
- stop the pathogen from spreading further

CANKER:
- A sunken necrotic lesion
- in the woody tissue e.g stem or branch
- Causes death of the CAMBIUM TISSUE in the bark

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20
Q

NON-SPECIFIC defences against pathogens in humans

A
  • RAPID
  • Prevent pathogens from gaining access to the body
  • Are the SAME for ALL pathogens

INCLUDE:
- skin
- mucous membrane
- expulsive reflexes
- blood clotting
- inflammation

OTHERS:
- Wax ~ in ear canal traps pathogens
- Acidic conditions ~ vagina

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21
Q

Skin

A
  • Provides a PROTECTIVE layer for the majority of the body surfaces
  • Outer layer ~ EPIDERMIS , consists of LAYERS of cells , mostly…

KERATINOCYTES :

  • produced by MITOSIS at the base of the epidermis
  • MIGRATE out to the surface of the skin
  • Dry out and the CYTOPLASM is replaced by the protein KERATIN.
  • Process ~ KERATINISATION
  • The keratinised layer of DEAD cells acts as an effective BARRIER to pathogens
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22
Q

Mucous Membrane

A
  • PROTECTIVE layer that lines openings such as trachea in the breathing system.
  • Secrete MUCUS which traps microorganisms , these can then be destroyed by PHAGOCYTES
  • In the STOMACH , the mucus contains HCl which helps to kill any pathogens in food or water
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23
Q

Lysozymes

A

MUCOUS MEMBRANE:
- Destroys BACTERIA by digesting the bacterial cell wall

TEARS:
- Prevents pathogens from entering the eye

Also found in SALIVA & LYSOSOMES

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24
Q

Expulsive Reflexes

A
  • pathogens can enter through openings e.g mouth or nose
  • Areas prone to attack are SENSITIVE and respond to irritants like toxins with reflexes including:
  • Coughing
  • Sneezing
  • Vomiting
  • Diarrhoea
  • These SUDDEN EXPULSIONS carry the microorganisms & irritants with it.
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25
Blood clotting
PLATELETS: - Tiny, short-lived, fragments of cells with no nucleus - Formed continuously in the bone marrow - Damage to the blood vessel wall EXPOSES COLLAGEN - The platelets are ACTIVATED : - form a PLUG over the damaged area - release CLOTTING FACTORS e.g thrombokinase - THROMBOKINASE together with Ca2+ ions act on a blood protein called PROTHROMBIN - Converted into an ACTIVE enzyme called THROMBIN - which acts on a SOLUBLE protein called FABRINOGEN - This CATALYSES the formation of INSOLUBLE FIBRIN which forms a MESH , which traps red blood cells to form a BLOOD CLOT.
26
What occurs after the BLOOD CLOT forms?
- The clot DRIES to form a SCAB - This PROTECTS the underlying tissue from pathogens while the wound heals - SKIN CELLS under the scab DIVIDE & REPAIR the damage - Scab FALLS OFF leaving freshly repaired skin
27
Inflammation
- When tissue is damaged, MAST CELLS are activated, releasing HISTAMINE. This causes: VASODILATION: - Blood vessels dilate or widen - increases the supply of blood to the effected area - causes area to feel HOT and RED - The increases in temperature reduces the ability of pathogens to REPRODUCE BLOOD VESSEL PERMEABILITY: - allows more blood plasma to leave the blood and form TISSUE FLUID - Causes nearby tissue to swell (OEDEMA) and feel PAINFUL. EXCESS TISSUE FLUID: - drained into the lymphatic system where lymphocytes are stored - The ACTIVITY of these lymphocytes... - causes swelling of the LYMPH NODES
28
Types of WHITE BLOOD CELL
Non-specific defences: PHAGOCYTES~ - Neutrophils - Macrophages ( also play a role in specific immune system) Specific defences: LYMPHOCYTES~ - B - T
29
OPSONINS
PROTEINS that attach to FOREIGN molecules and TAG them a foreign. - Include ANTIBODIES as well as other molecules which are called COMPLEMENTS. - The surface of pathogens are covered with chemicals - These FOREIGN CHEMICALS are what opsonins recognise , STICK TO , and tag.
30
Phagocytosis with NEUTROPHILS
- Neutrophil is ATTRACTED to molecules produced by pathogens ~ CHEMOTAXIS - RECEPTORS on the neutrophil MEMBRANE now attach to the opsonins - Pathogen is ENGULFED by ENDOCYTOSIS forming a PHAGOSOME - LYSOSOMES move towards the phagosome and FUSE with it , forming a PHAGOLYSOSOME. - HYDROLYTIC enzymes DIGEST pathogen - The HARMLESS products can be absorbed into the cell
31
Phagocytosis with MACROPHAGES 1
- Travel in the blood as MONOCYTES - The foreign molecules on the bacterium surface are ANTIGENS - Pathogen is ENGULFED into a PHAGOSOME - LYSOSOMES join to form a PHAGOLYSOSOME - HYDROLYTIC ENZYMES digest the pathogen
32
Phagocytosis with MACROPHAGES 2
ANTIGEN PRESENTATION: - The antigen is NOT fully digested, but moves to a PROTEIN COMPLEX on the surface of the cell - the antigens are presented to the EXTERIOR of the cell. - The macrophages are functioning as an ANTIGEN-PRESNETING CELL ( also play a critical role in the SPECIFIC immune system when presenting antigens to lymphocytes)
33
Cytokines
- CHEMICAL released by PHAGOCYTES when it engulfs a pathogen - SIGNALS to phagocytes and other IMMUNE CELLS to move to the site of infection - Also trigger INFLAMMATION & FEVER
34
The SPECIFIC immune response
- Responds to each pathogen in an INDIVIDUAL way - If it encounters the same pathogen again, it will produce a MORE EFFECTIVE response
35
Antigens
- MOLECULES e.g proteins or polysaccharides - On the SURFACE of all cells - The immune system can detect antigens on antibodies and sees them as FOREIGN or NON-SELF - This leads to an immune response ~ antibodies will be produced which specifically bind to the antigen - Does not apply to antigens on the surface of OUR body cells
36
STRUCTURE of ANTIBODIES
- Glycoproteins with 4 polypeptide chains - Two long , heavy chains that are identical to each other - Two shorter, light chains that are identical to each other - DISULFIDE BRIDES ~ hold the chains together HINGE REGION : - Provides flexibility - allows the distance between the two antigen binding sites to vary - makes it easier for two antigens to bind at the same time - ANTIGEN BIND SITES ( two)
37
Constant & Variable region of an antibody
CONSTANT: - Has the same structure for every antibody - no matter which B lymphocyte produced it. - Allows RECOGNITION by phagocytes VARIABLE: - Allows antigen to BIND - around 110 amino acids long on each chain - form the antigen binding sites - the shape is different for the antibodies produced by different B lymphocytes - The antibodies produced by different B lymphocytes will bind to different antigens
38
The SPECIFICITY of antibodies
-Two variable regions = Two antigen binding sites - allows bind to more than one of the SAME antigen - When an antigen binds, it is known as a antigen-antibody complex - The TERTIARY structure of the antigen-binding site is COMPLEMENTARY to the structure of the antigen
39
FUNCTIONS of antibodies
OPSONINS: - a group of antibodies - act as a binding site for phagocytic cells, so they can easily bind and destroy pathogen NEUTRALISATION: - Block antigen - bind to toxins ~ antitoxins - prevent entry to host cell AGGLUTINATION: - Bind together many pathogens - Now too large to enter host cell - More pathogens can be consumed by a phagocyte at once
40
Lymphocytes
- type of white blood cell - play an important part in the specific immune response - SMALLER than phagocytes - LARGE nucleus that fills most of the cell - Produced in the BONE MARROW before birth TWO types of lymphocytes , with different modes of action: T-lymphocytes (T cells) B-lymphocytes (B cells)
41
T lymphocytes
- Cell mediated immunity - Produced in the BONE AMRROW - Mature in the THYMUS GLAND T CELL RECEPTORS: - on the surface membrane of T lymphocytes - attach to an antigen - unique to each T lymphocyte
42
Cell - mediated response & role of T helper cells
- An ANTIGEN PRESENTING CELL , e.g macrophage, displays the antigen on its surface - This can be RECOGNISED by a TL with a T cell RECEPTOR that is COMPLEMENTARY to the antigen. T HELPER CELLS: CLONAL SELECTION ~ attach to surface antigens and are activated CLONAL EXPANSION (proliferation) ~ undergo mitosis, producing identical clones. Produce CYTOKINES called INTERLEUKINS: - trigger macrophage to increase their rate of phagocytosis - Stimulate B cells to undergo clonal expansion - Activate cytotoxic/killer cells DIFFERENTIATION ~ clones of the lymphocytes develop into a range of useful cells.( flashcard 43)
43
Clones of the T lymphocytes DIFFERENTIATE into:
CYTOTOXIC/KILLER T CELLS: - identify abnormal or virally-infected cells - attach to cell - Release protein, PERFORIN ~ forms holes in the membrane and triggers the destruction of the cell. T MEMORY CELLS: - Long-lived - Rapidly differentiate into killer T cells if the body is infected with the same pathogen again.
44
HUMORAL IMMUNITY & role of B lymphocytes
- Pathogen encounters the BL with the correct antibody to bind to the antigen on the pathogens surface - BL attaches to & engulfs pathogen by ENDOCYTOSIS - Pathogen is DIGESTED and antigens are presented on the surface of the BL ~ ANTIGEN PRESENTING CELL CLONAL SELECTION ~ T cell receptor from TL attaches to antigen on BL surface INTERLEUKINS ~ produced by TL activate BL to undergo mitosis CLONAL EXPANSION ~ clones of two types of cells are formed: PLASMA: - Release identical antibodies B MEMORY : - If a second infection occurs... - Rapidly differentiate into plasma cells - provide long term immunity
45
B lymphocytes
- HUMORAL IMMUNITY - Formed & mature in the BONE MARROW Antigen receptors: - attached to their surface membrane - these are membrane-bound ANTIBODIES - all of the antibodies on a particular BL will bind to the same antigen
46
ACTIVE IMMUNITY
Involves the activation of the persons OWN immune system: - B & T lymphocytes - Production of antibodies - The formation of memory cells ARTIFICIAL ACTIVE IMMUNITY: - Immune system is stimulated by dead or inactive pathogen by a VACCINATION NATURAL ACTIVE IMMUNITY: - A person is infected with a pathogen and produce their own antibodies
47
PASSIVE IMMUNITY
- The persons own immune system is not activated NATURAL PASSIVE IMMUNITY: - Babies receive antibodies from the mother through the placenta & breast milk ARTIFICIAL PASSIVE IMMUNITY: - Someone with TETANUS cannot produce antibodies quick enough - inactivated tetanus toxin injected into HORSE and antitoxin antibodies extracted - injected into patient
48
Why are new drugs needed?
- NEW diseases are emerging - Still many diseases with NO effective TREATMENTS - Many bacteria have EVOLVED ~ existing antibiotics are becoming LESS EFFECTIVE
49
Antibiotics & their Effects
ANTIBIOTICS ~ chemicals used to treat diseases caused by BACTERIA PENICILLIN: - First commonly used antibiotic - Discovered accidentally by Alexander Fleming - Produced by a type of FUNGUS Different antibiotics have different effects on bacterial cells: - break down peptidoglycan cell wall - target ribosomes , inhibiting protein synthesis
50
Why should biodiversity be preserved to help with the development of drugs?
- Plants & microorganisms are an important SOURCE of medicine - ASPIRIN discovered in WILLOW TREES - DIGOXIN discovered in FOXGLOVES - The destruction of their habitats, could lead to the loss of many UNDISCOVERED POTENTIAL MEDICINES
51
Personalised medicine
- Each person responds slightly differently to treatments due to GENETICS - E.G some people have ALLELES which cause their body to break down drugs more rapidly - This can affect the OPTIMUM DOSAGE of the drug needed to treat a patient IN THE FUTURE: - Analyse a persons GENOME - Allele variations can be determined - Best drug treatment can be decided for that person
52
What are VACCINES?
- Trigger a person to develop IMMUNITY to a pathogen - An example of ARTIFICIAL ACTIVE immunity - uses to prevent both EPIDEMICS (specific location) and PANDEMICS (continent or global) - Given via MOUTH or INJECTED into blood stream - Contain ANTIGENS from the pathogen that we want to protect the body against
53
Different FORMS of vaccines
ATTENUATED OR WEAKENED STRAIN OF A BACTERIUM OR VIRUS: - infects the patient - easily fought off by the immune system DEAD BACTERIAL CELLS OR INACTIVATED VIRUS: - the pathogen does not cause infection - antigen can still trigger an immune response ONLY ANTIGEN MOLECULES: - extracted from the pathogen - or manufactured using genetic engineering MODIFIED TOXIN MOLECULES: - these modifications make the toxin harmless but still allow it to act as an antigen
54
What happens once the vaccine has entered the human body?
PRIMARY RESPONSE IS STIMULATED: - production of antibodies & B memory cells - activation of T lymphocytes SECONDARY RESPONSE IS STIMULATED: - if the same pathogen re-enters the body - large amount of antibodies produced rapidly - the pathogen is destroyed before any symptoms develop
55
HERD immunity
In a population not everyone is vaccinated, e.g: - very young people - those with weakened immune systems - 85-99% of the population is vaccinated , meaning they are IMMUNE, controlling the spread - Those who are immune cannot pass the pathogen to the unvaccinated person
56
Why are people revaccinated?
Example~ INFLUENZA VIRUS - MUTATES regularly - ANTIGENIC VARIABILITY ~ changes it surface antigens - UPDATED vaccines have to be given
57
RING vaccination
- Used when a new case of a disease is reported - Those in IMMEDIATE VICINITY of the new case are vaccinated - TARGETS those who are MORE LIKELY to encounter the pathogen
58
What is an AUTOIMMUNE disease?
- When B & T lymphocytes mature , they are tested against SELF-MOLECULES - Any lymphocytes that RESPOND , are DESTROYED - PREVENTS your immune system from targeting molecules apart of your OWN BODY. - This process can FAIL and the immune system ATTACKS its SELF MOLECULES (Autoimmunity)
59
Examples of autoimmune diseases & treatments
TYPE 1 DIABETES: - immune system attacks and destroys BETA cells - causes uncontrolled blood glucose concentration - Treatment ~ insulin injection/pump RHEUMATOID ARTHIRITUS: - immune system attacks molecules found in joints - leads to limited mobility & joint damage - Treatment ~ steroids LUPUS: - immune system attacks proteins in the nucleus in cells - affects skin and joints - Treatment~ painkillers IMMUNOSUPPRESSANT TREATMENT: - reduces activity of the immune system - Can be negative as reduces the body's ability to defend itself
60
CAUSES of autoimmune diseases
- Cause is NOT well understood - GENETICS play a role as appear to run in families - The immune system may OVERRACT to a pathogen and begin to attack its own tissues
61
ANTIBIOTIC RESISTANCE: - How it occurs - Examples - Ways to prevent it
HOW DO BACTERIA BECOME RESISTANT? - Random mutations are continually taking place - A bacteria may develop a mutation for antibiotic resistance - Antibiotic kills the non-resistant bacteria - Resistant bacteria survive & reproduce EXAMPLES: - Staphylococcus aureus ~ resistant to methicillin - C.difficile ~ resistant to a number of common antibiotics WAYS TO PREVENT ANTIBIOTIC RESISTANCE: - ensure patients take the full course - reduce the unnecessary overuse of antibiotics - reduce use in farming
62
Why can't ANTIBIOTICS be used to treat diseases caused by VIRUSES?
- Viruses use HOST CELLS to manufacture PROTEINS & REPRODUCE - DO NOT contain any TARGET molecules for antibiotics to act upon. - Use ANTIVIRAL drugs instead

Biology (14 decks)

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