Module 4 Flashcards
What is a communicable disease?
illnesses resulting from the infection, presence and growth of pathogens in an individual host
What is a pathogen?
a disease causing organism which takes nutrition, energy and protection from and damages its host. (parasite)
What type of cell is bacteria? How are they classified?
prokaryotes classified by shape- rod (bacilli), spherical (cocci), comma shaped (vibrios), spiralled (spirilla) and corkscrew (spirochaetes)
By cell walls- 2 main types have different structures that react differently to gram staining Gram positive- look purple/ blue and Gram negative look red. The cell wall affects how they react to antibiotics
What is the chain of infection?
infective agent (pathogen)- bacteria, virus, protoctists, fungi
source of infection- the reservoir is the location of the microorganism which must meet needs of pathogen to grow and survive
mode of transmission- direct (skin to skin, bodily fluids) or indirect (pathogen transferee to intermediate that’s not infected but transfers pathogen to host (airborne droplets, insects)
susceptibility of host- young, elderly and those with underlying health conditions often have weaker immune systems
Are viruses living?
What structure do they have?
How do they replicate?
How do they evolve?
What are bacteriophages?
non living and very small
Have DNA/RNA surrounded by a protein
they invade living cells and their genetic material takes over the biochemistry of the host to make more viruses
They evolve my adapting to their host
They can even attack bacteria, using them to replicate and killing them at the same time
What type of cell are protocista? How do they infect?
Eukaryote parasitic using people/ animals as host
What type of cell are fungi?
what is their cell wall made of?
How do they absorb nutrients?
what type of fungi are pathogenic?
How do they affects plants?
How do they spread?
Eukaryote
cell wall of chitin
Can photosynthesise so digest food extracellularly before absorbing nutrients- saprophytic feeders. parasitic ones are as they live off organic matter
stop them photosynthesising as they affect the leaves
when they reproduce they produce millions of tiny spores
Bacterial animal disease
- Name of pathogen
- method of transmission
- symptoms/ method
- Tuberculosis
- mycobacterium tuberculosis
- Direct- droplets through air
- Lung tissue destroyed, immune system suppressed, coughing, fever, fatigue
- Bacterial meningitus
- Neisseria meningitidis, haemophilis influenzae
- direct- droplets though air and exchange of fluids In meninges (tissue surrounding brain to prevent entry of bacteria) of brain but can spread causing blood poisoning and death. Blotchy red rash that doesn’t disappear when a glass is pressed against it shows blood poisoning. Nausea, vomiting, fever, headache, muscle pain
Virus animal disease
- Name of pathogen
- method of transmission
- symptoms/ method
HIV/AIDS
- Human immunodeficiency virus (HIV)
- Direct- contact with bodily fluids, mother to child in breast milk
- Targets T cells in immune system and contains enzyme reverse transcriptase which transcribes RNA to a single strand of DNA in the host cell. HIV is a retrovirus as the process is opposite to usual.
- Flue like illness, fatigue, join and muscle pain
Influenza
- Influenza A, B and C
- Direct- droplets in air
- Sudden fever, body ache, fatigue, dry cough, kills cilia allowing airways to be infected
Protoctist animal disease
- Name of pathogen
- method of transmission
- symptoms/ method
- Malaria
- Plasmodium falciparum
- indirect- female anopheles mosquito.
- reproduce in mosquito then invade red blood cell then liver
- High temperature, headache, vomit, muscle pain, diarrhea
Fungus animal disease
- Name of pathogen
- method of transmission
- symptoms/ method
Cattle ringworm
- Trichophyton verrucosum
- Direct- contact with infected cattle
- grey white areas of skin with ashy circular areas. may be itchy
Athletes foot
- Epidermophyton floccosum, trichopyton rubrum, T. Mentagrophytes
- direct- contact with towels used by infetced people.
- Grows on and digests warm moist skin between toes causing cracking and scaling- itchy and sore
Bacterial plant disease
- Name of disease
- host plant
- names of pathogen
- Method of transmission
- Symptoms
- Ring Rot
- Potato, tomato
- clavibacter, michiganensis
- Direct contact with infected tubers, cultivation spreads it as bacteria remain of machinery damages leaves, tubers and fruit. Infects vascular tissue and blocks them so no water can enter leaves. Once a field is infected can’t grow potatoes for 2 years
Viral plant disease
- Name of disease
- host plant
- names of pathogen
- Method of transmission
- Symptoms
- mosaic
- Tobacco Tobaco mosaic virus (TMV)
- direct- contact with leaves of infected plants
- indirect- via aphids as vectors
- damages leaves, flowers and fruit, stunting growth. Yellow mosaic pattern on leaves. spreads though plasmodesmata and phloem
Fungus plant disease
- Name of disease
- host plant
- names of pathogen
- Method of transmission
- Symptoms
Black sigatoka
- bananas
- mycosphaerella fijiensis
- direct- spores are dispersed through air and spores germinate and grow into leaf through stomata. they are also present in soil
- indirect- fungus on infected plant releases spores and an insect eating the plant picks up the spores and transmits to other plants when it feeds
- yellow spots and black streaks. Hyphae penetrate and digest cells so leaves go black as can’t photosynthesise
Protocist plant disease
- Name of disease
- host plant
- names of pathogen
- Method of transmission
- Symptoms
- late blight
- potato, tomatoes
- phytophthora infestans
- direct- swimming zoospores and aerial spores
- hyphae penetrate host cells and destroy leaves, tubers and fruit.
- Blue/ grey spots, shrivel and go brown
disease transmission
why is it not always successful?
the transfer of pathogens from an infected host to an uninfected one
large numbers of pathogen produced to reach chances of reaching a host
infective stages are small to avoid wasting energy
Direct transmission:
CONTACT: between individuals TMV, RINGROT, RINGWORM kissing or bodily fluid contact HIV, microorganisms from faeces transmitted to hands
SPORES: BLACK SIGATOKA, LATE BLIGHT. Insects carry spores so could be indirect
INGESTION: contaminated food and drink, mouth to hands
ANIMAL BITES/ PUNCTURE WOUNDS (inoculation)
Indirect transmission:
VECTORS:
- wind carries spores
- water allow spores to swim in surface film of water on leaves
- animals carry pathogens and spores from one plant to another when they feed
- humans transmit pathogens and spores by hands, clothing, farming, transporting plants around the world
MALARIA, TMV
DROPLETS: of saliva and mucus in the air when you cough, sneeze and talk contain pathogens and can be inhaled by others
TB, MENINGITIS, FLU
FOMITES: inanimate objects transfer pathogens like door handle and towel
ATHLETES FOOT
WATER maybe soil
Factors affecting direct transmission animals and plants:
Animals/ human: close proximity like schools, hospitals and cramped housing- poverty
Plant: High density monocultures of crop plants
Factors affecting indirect transmission animals and plants:
climate and weather- damp and warm is good for vectors, especially mosquitos. Aphids and mosquitos need 20*c and over. Climate change worsens this as increased rain and wind increases spread, animals vectors are spread to new areas, but drier conditions in some areas could reduce spread there
Factors that affect transmission of human diseases
- poor nutrition
- compromised immune system
- poor waste disposal creates breeding sites for vectors
- culture and infrastructure- medical practices socioeconomic- lack of trained HC workers
- warning when outbreak
- poor sanitation and sewage
- housing contaminated water
- travel and migration bring diseases to populations with no natural resistance or immunity behaviour
- sexually transmitted diseases can be lowered depending on number of partners
Preventing spread of plant diseases:
leave space between plants
rotate crops (bacteria/spores die if no host)
strict hygiene- wash hands, boots machinery control insect vectors ?????
plant crops less susceptible to disease
plenty of minerals so healthier plants with more tolerance to infection
retrovirus
a virus like HIV with single stranded RNA as its genetic material, not DNA. when the retrovirus invades a host cell it uses its enzyme reverse transcriptase to make DNA from RNA template. Other RNA viruses like influenza don’t use their RNA as a template for making DNA
what is a vector:
an organism that transfers a pathogen from an infected host to an uninfected host and is not harmed by the pathogen itself
protoctist definiton
a eukaryotic unicellular organism
epidemic
endemic
pandemic
widespread occurrence of infectious disease in community at a particular time
a disease or condition regularly found in particular people/ place
a disease prevalent over a whole country or world
Comparing primary defences in plants and animals:
permanent physical barrier against infection:
prevent entry of pathogens:
Block movement of pathogens:
Use chemicals:
cellulose cell walls, skin
stomata closing, blood clots around open wound in skin
tyloses and calls, musus and cilia to remove
terpenes, HCL and lysosomes to kill pathogens
first line of defence
physical and chemical defences that prevent entry of pathogens into the body
Non specific defences
work the same way whatever the pathogen and are present from birth
How does the skin work as a primary defence?
- Impermeable to most pathogens with a keratinised layer of dead epithelial cells. - Hostile conditions as lactic acid and fatty acids are secreted from sweat and sebaceous glands are acidic. When sweat evaporates it leave salty, dry conditions combined with low pH prevent microorganisms growing and multiplying. - Skin floral healthy microorganisms that outcompete pathogens for space on surface. Also inside body like intestines
Primary defences
skin
mucous membranes
expulsive reflexes
other
Mucous membranes
Line parts of the body likely to come into contact with pathogens eg. airways, digestive tract, genital tracts mucous is secreted by goblet cells in the epithelium and traps pathogens its sticky because its full of glycoprotein molecules which have long carbohydrate chains and contains antimicrobial enzymes cilia on ciliated epithelium in airways waft mucus up where it is swallowed
Expulsive reflexes
coughing and sneezing ejects pathogen-laden mucus from gas exchange system areas prone to infection are sensitive to dust, microorganisms or the toxins they release ? happen automatically to expel foreign bodies
Other primary non specific defences:
lysozymes destroy bacterial and fungal cell walls and are found in blood, sweat, tears and phagocytes remove remaining pathogens.
acidic conditions of stomach and vagina kill pathogens
non pathogenic bacteria live in our digestive/ genital tract and compete with invading organisms
ear canal lined with wax
vomiting and diarrhoea expel contents of gut along with any infective pathogens
what types of defence is blood clotting?
Why is it needed?
Why is the process so complex?
How is it activated?
What is involved?
Name the order of enzymes:
- second line non specific
- Blood clotting is required to provide a temporary seal to prevent infection as if skin is breached pathogens can enter the body
- to avoid clotting where its not needed
- When platelets come into contact with collagen in skin or wall of damaged blood vessel they adhere and begin to secreted several substances
- clotting factors which activate an enzyme cascade (product of one reaction activates the next)
- Thromboplastin converts inactive protease to active protease. Ca2+ catalyst helps prothrombin convert to thrombin which converts soluble fibrinogen to insoluble fibrin. This forms a clot with traps platelets and blood cells, then dries to form a scab.
Apart from the thromoplastin cascade, what is the other clotting method?
serotonin makes the smooth muscle in the walls of the blood vessels contract so they narrow and reduce the supply of blood to the area
What is the second stage of wound repair?
- layer of fibrous collagen starts to form under the scab to give new tissue strength
- granulation tissue fills the would allowing further changes to occur underneath
- The outer layers of stem epidermal cells divide by mitosis, into skin cells and migrate to the edge of the wound.
- Platelets secrete growth factors that attract cells to divide and grow
- The tissue then contracts to draw the edges of the wound together
- new blood vessels form to supply nutrients to the tissue
- death of unwanted cells
- scab falls of once new epidermis reaches normal thickness
Secondary defences
phagocytic and antimicrobial cells that act against the type of microorganism that has breeched the primary defences non specific
inflammation definition What are the signs?
the local response to tissue damage and infection, involving the release of chemical signalling molecules and resulting in an increased blood flow and movement of phagocytes into the infected tissue swelling (oedema), pain, heat and redness
Inflammation process
- Damaged/infected tissue releases histamine molecules from mast cells which increase permeability of blood capillaries.
- Fluid leaks into surrounding tissue fluid which is what causes swelling and pain and phagocytes can leave the blood and enter infected tissues.
- The histamine also cause vasodilation which makes the area hot and brings lots of white blood cells. The raised temperature also helps prevent pathogens reproducing.
- When excess tissue drains into lymphatic system the specific immune response is initiated
- Histamine stimulate infected cells to secrete cytokines. Cytokines (including interleukin) stimulate defences in affected area including binding proteins to material to be digested by phagocytes (these proteins can increase 1000x at the start of an infection!). They also promote inflammation and cause the liver to release acute phase proteins, some of which bind to the surfaces of bacteria and damaged host cells to promote phagocytosis. These signalling molecules are also responsible for causing fever and sleepiness by stimulating the brain
Fever- how does it occur Why is it good?
hypothalamus in brain maintains 37*C. when a pathogen invades, cytokine stimulate the hypothalamus to reset the thermostat and temperature goes up. This inhibits pathogen reproduction and the specific immune system works faster at higher temperatures.
What is a passive defence?
What are the passive plant defences- split into physical and chemical?
there all the time
Physical:
- waxy cuticle over leaf epidermis- stops virus and bacteria entering through wounds made by herbivores
- Casparian strip in root endodermis- stops fungi entering through roots
- bark
- cellulose cell walls
- stomatal closure
Chemical:
- secreting toxic compounds- phenols
- secreting enzyme inhibitors that inhibit enzymes needed for plants to enter the plant- tannins
- Sticky resins in bark prevent spread
- secreting compounds which support growth of microorgainsims that are competitors of pathogens
- receptor molecules on cell surface membranes detect pathogens and activate plant defences
Active plant defences
- Hypersensitivity/ necrosis Immediate death of tissue surrounding infection site to prevent spread of infection. Many pathogens require a living host tissue to survive for energy and nutrients used for growth
- Callose deposition Callose is a large polysaccharide that blocks sieve tubes (phloem) or plasmodesmata preventing the spread of the pathogen. Also deposited in sieve pores to block the transport of phloem sap and impede pathogen movement. Cells walls have it too, along with antimicrobial compounds like hydrogen peroxide
- Tyloses growths that block the xylem by swelling preventing pathogen spreading through plant. they are filled with plant chemicals called terpenes
- Cell signalling using signalling molecules like salicylic acid activate defence mechanisms in uninfected areas. They then have system acquired resistance for some time after the original infection if it returns. They produce defence chemicals- phytoalexins which:
disrupt cell surface membranes of bacteria
delay reproduction of pathogen
disrupt metabolism of pathogen
release chitinases to break down hyphae walls
Name a few plant chemicals we extract for use:
Why can’t plants produce cells that roam all over the body?
insect repellents- citronella from lemon grass
insecticides- caffeine is toxin to insects and fungi
fixed cell walls
What are phagocytes?
What are 3 phagocytes?
when and where are they produced?
what causes them to migrate?
what do they contain
specialised cells in the blood and tissue which engulf and digest pathogens and dead cells
neutrophils macrophages (monocytes) dendritic cells
throughout life by the bone marrow
signalling molecules from damaged cells
lysosomes (vesicle containing digestive enzymes)
What is the most common phagocyte?
what is a special feature of this phagocyte and why is it useful?
what happens during infections? What happens after they ingest bacteria? What is pus mostly made of?
neutrophil
lobed nucleus so they can leave capillary walls as more flexible
travel in blood and enter tissue fluid during infections, large numbers quickly released from bone barrow in infections
short lived- die after ingesting bacteria
dead neutrophils
What do macrophages do?
How are they different to neutrophils?
Where are they found?
where are they made?
consume and destroy any pathogens they encounter
larger and long lived, and initiate a specific immune response as they display antigens from the pathogens to lymphocytes
found in organs/ lymph not the blood. common in lungs as stuff enters there
bone marrow as monocytes (called macrophages once reach organs)
What is a special feature of dendritic cells?
where are they found?
what happens to them after phagocytosis?
have long processes to give a large surface area to interact with pathogens and lymphocytes and are antigen presenting cells (APC’s) like macrophages?
mainly found in areas near to surfaces like skin, digestive tract, mucous membranes
they migrate to the lymph nodes
Describe the process of phagocytosis include process of antigen presentation
- chemotaxis (phagocyte moves in response to chemicals produced by pathogens) and adherence of microbe to phagocyte. can recognise non human proteins on pathogen (not specific)
- ingestion of microbe to phagocyte by endocytosis and invagination
- formation of a phagosome (phagocytic vesicle)
- formation of a phagolysosome ( when lysosome fuses with phagosome)
- digestion of ingested microbe by enzymes from lysosome
- formation of residual body containing indigestible material
- discharge of waste materials my exocytosis and antigens from surface of pathogen absorbed so they can be displayed and used to tell lymphocytes which antibodies to make much quicker, without the real pathogen there to cause damage. The antigens from the pathogen surface membrane combine with special glycoproteins from cytoplasm called major hostocompatability complex (MHC) which moves them to the phagocyte surface membrane becoming APC
How does histamine increase effectiveness of phagocytes?
when cells are under attack they release histamine which makes capillaries more leaky so extra fluid in the blood leaves to become tissue fluid this means more fluid enters the lymphatic system, flushing pathogens towards the macrophages waiting in the lymph nodes so the specific immune response can begin sooner
When are cytokines released and how do they help phagocytes?
what do opsonins do and how do they help?
cytokines are released by a pathogen when it engulfs the phagocyte and they tell other phagocytes the body is under attack and stimulate them to move to the site of the infection
opsonins are chemicals eg. antibodies that bind to and tag the pathogen making it more easily recognised by the phagocyte they also bind to receptors on phagocytes membranes which help the pathogen be engulfed
3 features of antigens:
What do they do?
What are they specific to?
what is specific to antigens?
- proteins or glycoproteins
- large molecules
- have a specific shape on or in the cell surface membrane
they stimulate a immune response eg. production of antibodies
the organism
antibodies
What is another name for antibodies?
what produces them?
what structure do they have?
immunoglobulins
lymphocytes in response to an infection
globular proteins with 4 or more polypeptides
In the antibody structure: what is the function of the variable region?
What is the function of the hinge region?
what is the function of the constant region?
What are the light chains?
What are the heavy chains?
Where is the antigen binding site?
What bonds are involved?
it changes due to different sequence of aa giving it a different 3D shape so is specific for different antibodies
allows flexibility so the antibody can bind to 2 separate antigens
its the same for all antibodies of the same class, and is a receptor binding site on the phagocyte surface so it can detect pathogens labelled by antibodies for phagocytosis
2 smaller polypeptides on the outside
2 larger polypeptides on the inside
at the top of the y and involves all 4 polypeptides- there are 2 identical ones
disulphide bridges form between polypeptides and within polypeptides
What is it called when the antigen and antibody bind?
antigen-antibody complex
How do antibodies work?
Agglutination- antibodies bind to 2 identical antigens on 2 or more pathogens which makes them clump together so they are less likely to spread and and easier for engulfing. bigger antigens are better for this as there are more binding sites
Immobilisation- some attach to the bacterial flagella making them less active and easier for phagocytes to engulf
Opsonins- some act as these by acting as labels coating the pathogen so the phagocyte can identify it. The phagocytes have receptors for the constant region of antibodies
Some block the binding sites on the pathogen so its unable to bind to a host cell (neutralisation)
Antitoxins- they block toxins they are complementary to them so combine with them to make them harmless eg, for those causing diphtheria and tetanus
They also can attach to the membrane and puncture or burst it
Describe trend in graph and explain why for primary and secondary response
low numbers of antibodies in blood as there is a lag phase until antibodies are produced.
small and gradual peak which is short lived.
if the first infection passes the antibody concentration required for immunity then if a second infection occurs with the same pathogen the lymphocytes can quickly make the same antibodies again- the previous ones don’t stay in the blood.
immediate and stronger response shown by a steeper and higher peak.
Due to the presence of memory cells made during the response it is long lived. The graph declines slower too why long lived due to memory cells??
What is the specific immune system?
when lymphocytes and antibodies act against specific pathogens
What is the difference between the specific and no specific immune system?
specific is much slower as only have a small no of each as there are so many lymphocytes so there is a lag time between being infected and producing antibodies due to clonal selection and expansion
also not born with it but can produce when there’s an infection
Immune response
the sequence of events that occur as the specific immune system responds to foreign antigens involving activation of cloning of B cells and T cells specific to antigens
Where do B and T cells originate and mature?
stem cells in bone marrow where they differentiate into mature cells that spread out through the body’s lymphatic system in bone marrow but migrate to thymus gland to mature then spread across lymphatic system
What types of T cells are there?
What types of B cells are there?
T helper cells
T killer cells
T memory cells
T regulator cells
Plasma cells
B memory cells
What do T helper cells do?
have CD4 receptors on cell surface membranes which bind to surface of antigens on APC’s
produce interleukins when they bind- interleukin 1 produced by macrophage which enhances T cell activation, and T cell releases interleukin 2 which causes the proliferation of other helper T cells (positive feedback) and helps activate plasma cells and T killer cells
interferon may also be produced stimulating killer T cell activity
What do killer T cells do?
destroy pathogens and infected cells (they display antigens on surface)
produce chemical perforin which has proteins that channel through membranes so toxins can enter, killing the pathogen
What do T memory cells do?
part of immunological memory
have encountered specific antigens before so can respond quickly and strongly if that antigen is encountered again by dividing to form killer T cells
What do T regulator cells do?
control the immune system by stopping the immune response when no more antigens are present
they also make sure the body recognises self antigens so doesn’t set up an autoimmune response
What do B lymphocytes do?
produce antibodies to a particular antigen which inactivate circulating antigens
only live for a few days but produce 2,000 antibodies/ second
What do B memory cells do?
live for a very long time and provide immunological memory
remember a very specific antigen and if its encountered again they can rapidly differentiate into plasma cells
more antibodies are produced and they last longer