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
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
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
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
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
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
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
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
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
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
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