Module 3 of 3 · Text
Communicable diseases
Communicable diseases
- Types of pathogen
- bacteria
- prokaryotes
- classified by shape:
- rod = bacilli
- spherical = cocci
- comma shaped = vibrios
- spiralled = spirilla
- corkscrew = spirochaetes
- classified by cell walls and how they appear after gram staining:
- gram positive bacteria = purple-blue under light microscope --> MRSA
- gram negative bacteria = red under light microscope --> E.coli
- useful because it effects how they react to antibiotics
- viruses
- non-living infectious agents
- some genetic material surrounded by protein
- they invade living cells, hijack the biochemistry and make more virsuses
- reproduce rapidly and evolve by developing adaptations to their host
- there are even ones that attack bacteria called bacteriophages
- considered ultimate parasites
- proctoctista (protista)
- eukaryotic microorganisms with various feeding methods
- percentage act as pathogens for both plants and animals --> parasitic
- many need a vector to transfer them or they may enter the body through contaminated water
- fungi
- cause more devastation in plants
- eukaroyitc organisms but the ones that effect humans tend to be single-celled
- some are parasitic and feed on living plants and animals
- normally stop plants from photosynthesising
- bacteria
- Modes of action
- damaging the host tissues directly
- viruses take over cell metabolism --> make host cell create loads of copies of them then they burst out which destroys the cell
- some protoctista take over cells but don't take over genetic material they just digest the cell's contents when they reproduce
- fungi digest living cells and destroy them
- producing toxins
- most bacteria produce toxins that poison or damage host cells --> breakdown the membranes, inactivate enzymes or interfere with genetic material
- some fungi produce toxins
- damaging the host tissues directly
- Plant diseases
- ring rot
- effects tomatoes, potatoes and aubergines
- caused by gram positive bacteria
- damages leaves, tubers and fruit
- tobacco mosaic virus
- effects tobacco plants, tomatoes, peppers and cucumbers
- caused by virus
- damages leaves, flowers and fruit
- potato blight
- effects potatoes and tomatoes
- caused by protoctist
- destroys leaves, tubers and fruit
- no cure
- black sigatoka
- effects bananas
- caused by fungus
- penetrates and digests cells
- can cause 50% reduction in yield
- no cure
- ring rot
- Animal diseases
- tuberculosis
- bacterial disease
- damages lung tissue and suppresses immune system
- both curable and preventable in humans
- bacterial meningitis
- bacterial infection of meninges of the brain which can spread to the rest of the body
- mainly effects young children and teenagers
- antibiotics cure it if given early enough
- vaccines prevent it
- HIV/AIDS
- acquired immunodeficiency syndrome caused by human immunodeficiency virus
- HIV targets T cells in immune system
- gradually destroys immune system so people infected are open to other diseases (TB or pneumonia)
- HIV = retrovirus so infects the host cell, uses reverse transcriptase to make DNA from its own RNA which interacts with the host's DNA
- passed through bodily fluids
- no vaccine and no cure
- anti-retroviral drugs slow the process
- Influenza
- viral infection of ciliated epithelial cells in the gas exchange system (kills them which opens the airways to secondary infection)
- three main strains - A, B & C
- strain A are the most virulent and classified further by proteins on their surfaces
- mutate regularly
- vaccines available every year with the predicted variations
- no cure
- Malaria
- protoctista spread by bites of mosquitoes
- female mosquitoes bite for blood to get protein before she lays her eggs
- the protoctista invades the red blood cells, liver and brain
- the disease recurs making them weak and vulnerable
- no vaccine and limited cures
- need to control the vector / mosquitoes
- Ring worm
- fungus affecting mammals
- not damaging, just looks unsightly and is itchy
- antifungal creams clear it
- Athlete's foot
- human fungal disease
- form of ring worm that digests the skin between the toes
- antifungal creams cure it
- tuberculosis
- Transmission of pathogens between animals
- direct transmission
- direct contact (kissing, skin-to-skin contact, microorganisms from faeces transmitted on the hands)
- inoculation (break in the skin, bite, puncture wound)
- ingestion (contaminated food or drink)
- indirect transmission
- fomites (inanimate objects like bedding, socks or cosmetics)
- inhalation (droplets of saliva or mucus from coughing, speaking or sneezing)
- vectors (transfer communicable pathogens unintentionally)
- water acts as a vector
- factors affecting transmission
- overcrowded conditions
- poor nutrition
- compromised immune system
- poor waste disposal
- climate change can introduce new vectors and pathogens
- culture and infrastructure
- socioeconomic factors like a lack of trained health workers
- direct transmission
- Transmission of pathogens between plants
- direct transmission
- contact of healthy plant with infected one
- indirect transmission
- soil contamination (could leave reproductive spores in soil that infect next crop)
- vectors (wind - may carry any pathogen, water - spores float on the surface, animals - insects and birds carry pathogens and spores as they feed, humans - transmitted by contact)
- factors affecting transmission
- some vareities are suceptible to diseases
- overcrowding increases contact
- poor nutrition reduces resistance
- damp, warm conditions increase the survival of pathogens
- climate change - increased rainfall and wind promote the spread of pathogens
- direct transmission
- Plant defences against pathogens
- recognising an attack
- receptors in cells respond to molecules from the pathogens or chemical produced when cell wall is attacked
- stimulates signalling molecules which trigger responses like production of defensive chemicals, sending alarm signals to uninfected cells and physically strengthen the cell walls
- physical defences
- callose is synthesised and deposited in the cell walls and membranes to act as barriers around site of infection
- large amounts of callose continue to be deposited in the cell walls and lignin is added to make the barrier thicker and stronger
- callose blocks sieve plates of phloem to cut off infected region
- callose is deposited in plasmodesmata to seal the cell off from healthy cells
- chemical defences
- insect repellents
- insecticides
- antibacterial compounds containing antibodies
- antifungal compounds with chitinases which interfere with fungi membranes
- anti-oomycetes with glucanases which breakdown glucans found in cell walls of oomycetes
- general toxins
- recognising an attack
- Non-specific animal defences
- skin - produces sebum, an oily substance than inhibits the growth of pathogens
- most body tracts are line by mucous membranes that secrete mucus to trap microorganisms (also contains lysozymes and phagocytes)
- tears, stomach acid and urine contain lysozymes
- expulsive reflexes (coughing and sneezing)
- blood clotting
- platelets come into contact with collagen in skin or blood vessel walls
- platelets adhere and secrete thromboplastin and sertonin
- thromoplastin catalyses the production of thrombin which catalyses the production of fibrin which forms the clot
- sertonin causes vasoconstriction to reduce blood flow to the area
- scars from when to much collagen is used to stitch the wound back up
- inflammatory response
- mast cells are activated by damaged tissue
- mast cells release cytokines and histamines
- cytokines attract white blood cells to the site
- histamines cause vasodilation to increase the temperature (stops pathogen reproduction) and increases the permeability of blood vessels so the increased tissue fluid is used to restrict the pathogen
- fevers
- high temperatures inhibit pathogen reproduction
- specific immune system works faster at higher temperatures
- phagocytosis
- pathogens produce chemicals that attract phagocytes
- they recognise the pathogen's antigens as non-self
- they engluf the pathogen and enclose it in a phagosome
- the phagosome then fuses with a lysosome to make a phagolysosome
- the enzymes in the lysosome digest the pathogen
- when a macrophage englulfs a pathogen it combines the antigens with its MHCs (major histocompatibility complexes) aka special glycoproteins in its plasma membrane --> forms a APC (antigen-presenting cell) which stimulates the specific response
- helpful chemicals
- cytokines cell-signal other phagocytes into helping out in the infected region + increase the body temperature
- opsonins bind to pathogens to tag them for phagocytes (bind to protein in the phagocytes membranes)
- Specific immune response
- antibodies
- Y shaped glycoproteins aka immunoglobulins that bind to a specific antigen or toxin
- two identical long heavy chains bound to two identical short light chains with disulfide bridges
- the binding site is at the end of the light chains aka the variable region
- rest of the atibody is the same on all of them so = constant region
- the hinge region where the heavy binds to light chains gives it flexibility to bind to two antigens at once
- forms antibody-antigen complexes
- they help by:
- complex acts as an opsonin
- most pathogens are no longer effective when its bound to antigens
- act as agglutinins which clump pathogens together
- act as anti0-toxins
- lymphocytes
- T helper cells --> have receptors on their membranes that bind to the antigens on the APCs; they produce interleukins (type of cytokine) which stimulate the activity of B cells
- T killer cells --> destroy pathogens with perforin which increases their membrane permeability so the pathogen cell leaks
- T memory cells --> part of the immunological memory (when they meet the pathogen again they quickly divide and handle it fast)
- T regulatory cells --> suppress the immune system to control and regulate it
- Plasma cells --> produce antibodies for the particular antigen
- B effector cells --> divide to form plasma cell clones
- B memory cells --> part of the immunological memory (remember specific antibody needed for that antigen)
- cell mediated immunity
- phagocyte englufs pathogen to become an APC
- receptors on T helper cells fit the antigen
- T helper cell is the replicates by clonal expansion --> the clones differentiate into T helpers, T killers, T regulatory cells, and T memory cells --> also releases interleukins to stimulate more phagocytosis
- humoral immunity
- APCs = B cells
- interleukins produced by the activated T helper cell attracts B effector cells
- B cells have antibodies in their membrane - when the right antibody binds to the antigen on the APC it undergoes clonal expansion
- clonal expansion of B cell results in plasma cells and B memory cells
- plasma cells release a load of antibodies into the blood to help fight the infection
- antibodies
- Autoimmune diseases = when the T regulatory cells don't work properly so the immune system continues its attack but on self cells
- type 1 diabetes, arthritis, lupus
- Natural immunity
- active = when the body itself acts to produce antibodies and memory cells
- passive = breast feeding passes antibodies from mother to baby *first milk is most important aka colostrum*
- Artificial immunity
- active = vaccinations (prevent epidemics)
- passive = antibody injections
- Medicines and the management of diseases
- sources of medicines
- penicillin comes from a mould
- scientists design drugs on complex comupter programmes
- analysis of the genomes of pathogens to find vulnerabilities
- sources of medicines
- Drug design for the future
- pharmacogenetics
- personalised medicine where the drugs work with your individual combination of genetics and disease (look at genome of patient and genome of pathogen)
- synthetic biology
- using genetic engineering we can develop populations of bacteria that produces drugs that are otherwise very rare, too expensive or not available
- mammals also used to produce drugs in their milk (pharming)
- nanotechnology uses tiny non-natural particles that are used for biological purposes
- pharmacogenetics
- The antibiotic dilemma
- antibiotics work through selective toxicity where bacterial cells but not body cells are affected
- over-prescriptions of antibiotics mean that some bacteria have built up resistance to the,
- antibiotic resistant bacteria include MRSA and C. difficile which cause real issues in hospitals and care homes
- antibiotic resistance can be reduce long-term by:
- minimising the use of antibiotics
- ensuring every course is completed fully
- good hygiene in care homes, hospitals and in general