Communicable Disease Flashcards
What are communicable diseases?
- Can be spread between organisms of the same species or sometimes between different species.
- Spready by PATHOGENS
What are PATHOGENS?
microorganisms which can causes disease.
- HOST ~ the organism which the pathogen infects
FOUR main categories:
- bacteria
- virus
- fungi
- protoctista / protista
Bacteria
- 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
Examples of Bacterial diseases
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
Viruses
- 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
How do viruses REPRODUCE?
- 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
Examples of VIRUSES
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
Fungi
- 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
Examples of fungal infections
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
Examples of PROTISTA diseases
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
Protocista/ protista
- 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
Direct transmission and factors that affect these
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
SOCIAL FACTORS that affect transmission
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
Indirect transmission
Passing a pathogen from host to new host via a VECTOR.
VECTOR ~ an organism that carries a pathogen from one host to another
PASSIVE DEFENCES of plants against pathogens
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
Callose & Tylose formation
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
ACTIVE defences of plants against pathogens
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
CHEMICAL defences of plants against pathogens
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
Necrosis & Canker
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
NON-SPECIFIC defences against pathogens in humans
- 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
Skin
- 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
Mucous Membrane
- 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
Lysozymes
MUCOUS MEMBRANE:
- Destroys BACTERIA by digesting the bacterial cell wall
TEARS:
- Prevents pathogens from entering the eye
Also found in SALIVA & LYSOSOMES
Expulsive Reflexes
- 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.
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.
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
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
Types of WHITE BLOOD CELL
Non-specific defences:
PHAGOCYTES~
- Neutrophils
- Macrophages ( also play a role in specific immune system)
Specific defences:
LYMPHOCYTES~
- B
- T
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.
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
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
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)
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
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
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
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)
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
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
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
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)
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
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)
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.
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
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
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
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
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
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
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
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
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
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
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
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
Why are people revaccinated?
Example~ INFLUENZA VIRUS
- MUTATES regularly
- ANTIGENIC VARIABILITY ~ changes it surface antigens
- UPDATED vaccines have to be given
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
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)
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
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
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
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
