4.12 - Communicable diseases Flashcards
(80 cards)
1
Q
Bacilli (bacterial pathogens)
A
- Rod-shaped bacteria and archaea
- Rods (bacilli) or chains (streptobacilli)
- Salmonella (S. enterica)
- Anthrax (B. anthracis)
2
Q
Cocci
A
- spherical bacteria
- Mostly lack flagella and are non-motile
- Streptococcus pneumonia
- Staphylococcus aureus
3
Q
How are bacteria classified
A
Basic shape:
- bacilli, cocci, vibrios, spirilla, spirochaetes
Cell wall structure:
- gram positive bacteria look purple-blue under a light microscope following gram staining e.g. MRSA
- gram negative bacteria appear red following gram staining e.g. e.coli
- type of cell wall affects how bacteria react to different antibiotics
4
Q
Spirals
A
- Spirals (spirillum) or corkscrews (spirochaete)
- External (spirillum) / internal (spriochaete) flagella
- Campylobacter jejuni, Helicobacter pylori
5
Q
Vibrios
A
- Comma-shaped bacteria
- Motile with flagella
- Cholera (V. cholera)
- V. vulnificus
6
Q
Viruses
A
- 200-300nm
- non-living infectious agents
(acellular and cannot reproduce without a host) - a short section of RNA surrounded by protein.
- infect cells by inserting its own RNA into the DNA of a cell
- The infected cell will then begin to produce more viruses
- all natural viruses are pathogens
- affect all types of organisms, even bacteria, these are called bacteriophages
Examples include HIV, herpes, tobacco mosaic virus (TMV) and SARS-CoV-2
7
Q
Protoctista
A
- 5-3000μm
- diverse range of eukaryotic organisms
- vary widely in cellular structure, locomotion, life cycles and feeding methods
- Includes unicellular organisms, and cells grouped into colonies.
- Small percentage act as pathogens, causing disease in plants and animals
- Protists which are pathogenic are parasites – using host organisms
- may require a vector e.g. malaria (mosquito) and sleeping sickness (tsetse fly)
- May enter host directly through contaminated water e.g. amoebic dysentery and Giardia
8
Q
Fungi
A
- 5-50μm
- do not cause significant harm to animals, but can be devastating to plants
- eukaryotic organisms, which can be unicellular or multicellular without tissues
- Fungi that are human pathogens are unicellular e.g. thrush, ringworm
- Fungi cannot photosynthesise so digest food extracellularly before absorbing nutrients
- parasitic fungi are the fungal pathogens that cause disease
- can often affect leaves, preventing photosynthesis
- produce millions of spores, which enable them to spread widely and rapidly, particularly among crop plants
9
Q
The two modes of action of pathogens
A
Damaging the host directly:
- viruses take over the cell metabolism to make new viruses and then burst out of the cell, destroying it
- some protoctista take over cells and break them open, digesting the cell contents as they reproduce
- fungi digests living cells and destroys them. This combined with the body’s response to the damage gives symptoms of disease
Producing toxins which damage host tissues:
- bacteria produce toxins (a by-product of the normal functioning of bacteria) that damage the host in some way, causing disease. Some toxins break down cell membranes, damage or inactivate enzymes or interfere with the host cell genetic material
- some fungi produce toxins which affect the host cells and cause disease
10
Q
Ring rot
A
- a bacterial disease of potatoes, tomatoes and aubergines
- caused by gram-positive bacteria Clavibacter michiganesis
- damages leaves, tubers and fruit
- can destroy up to 80% of the crop
- there is no cure
- once bacterial rot infects a field it cannot be used to grow potatoes for 2 years
11
Q
Tobacco mosaic virus (TMV)
A
- a virus that affects tobacco plants and around 150 other species (tomatoes, peppers etc)
- damages leaves, flowers and fruits, stunting growth and reducing yields
- can lead to an almost total crop loss
- no cure, but resistant crop strains are available
12
Q
Potato blight
A
- caused by a fungus-like protoctist oomycete (Phytophthora infestans)
- hyphae penetrates host cells, destroying leaves, tubers and fruit
- causes millions of pounds worth of crop damage each year
- no cure, but resistant strains, careful management and chemical treatments can reduce infection risk
13
Q
Black sigatoka
A
- banana disease caused by a fungus (Mycosphaerella fijiensis)
- attacks and destroys leaves
- hyphae penetrate and digest the cells, making the leaves black
- causes 50% reduction in yield
- resistant strains are being developed
- good husbandry and fungicide treatment can control the spread of the disease but there is no cure
14
Q
Tuberculosis (TB)
A
- Droplet infection (inhalation)
- bacterial disease of humans, pigs, cows, pigs, badgers and deer
- commonly caused by Mycobacterium tuberculosis and M.bovis
- damages and destroys lung tissue and suppresses the immune system so the body is less able to fight off other diseases
- people affected by HIV/AIDS are more likely to develop TB infections
- curable by antibiotics
- preventable by improving living standards and vaccination
15
Q
Bacterial meningitis
A
- Droplet infection (inhalation)
- fomites via infection routes
- bacterial infection (Streptococcus pneumoniae or Neisseria meningitidis) on the meninges of the brain (protective surfaces on the surface of the brain)
- can spread to the rest of the body, causing septicaemia (blood poisoning) and rapid death
- mainly affects very young children and teenagers
- blotchy rash that does not disappear when a glass is pressed against it
- antibiotics will cure the disease if delivered early
- vaccines can protect against some forms
16
Q
HIV/AIDS
A
- acquired immunodeficiency syndrome (AIDS) is caused by human immunodeficiency virus (HIV)
- HIV targets T-helper cells in the immune system and gradually destroys it
- means affected people are open to other infections such as TB and some types of cancer
- can affect humans and some primates
- a retrovirus with RNA as its genetic material
- passed from person to person in bodily fluids (unprotected sex, sharing needles etc)
- no vaccine and no cure, but antiretroviral drugs slow progress of disease
- FGM increases infection rate
17
Q
Influenza (flu)
A
- Direct contact
- droplet infection (inhalation)
- fomites
- viral infection (Orthomyxoviridae) of ciliated epithelial cells in the gas exchange system
- kills them, leaving the airways open to secondary infection
- can be fatal for young children, old people and people with chronic illnesses (usually from secondary bacterial infections such as pneumonia)
- affects mammals and birds
- three main strains; A, B and C
- A viruses are the most virulent and also classified by proteins on surface
- mutate regularly, so you cannot be totally immune from year to year
- no cure, but vulnerable groups are given a flu vaccine
18
Q
Malaria
A
- caused by protoctista Plasmodium
- spread by the bite of infected Anopheles mosquitoes
- Reproduce inside female mosquitos and the parasite is passed to human hosts when the mosquito takes blood meals, invading red blood cells and liver
- Causes recurring fever and weakness, making hosts vulnerable to other infections
- Limited cures, no vaccine
- Vector controlled with habitat destruction and insecticides
- Prevent biting e.g nets
19
Q
Ring worm
A
- direct contact
- fomites e.g. bedsheets, soil
- fungal disease affecting mammals
- different fungi infect different species
- causes grey-white crusty infectious areas of skin
- not damaging
- antifungal creams are an effective cure
20
Q
Athlete’s foot
A
- direct contact
- fomites e.g. towels, floors
- form of human ringworm
- grows on and digests warm, moist skin between the toes
- antifungal creams are an effective cure
- causes cracking and scaling
- prevented by good hygiene
21
Q
Forms of direct transmission
A
Direct contact (contagious diseases):
- contact with the body fluids of an infected person
- skin-to-skin contact
- microorganisms from faeces transmitted on the hands
Inoculation
- through a break in the skin
- from an animal bite
- through a puncture wound
Ingestion:
- taking in contaminated food or drink or transferring pathogens to the mouth from the hands
22
Q
Forms of indirect transmission
A
Fomites:
- inanimate objects such as bedding can transfer pathogens
Droplet infection (inhalation):
- minute droplets of saliva and mucus expelled from mouth as you talk, cough or sneeze
Vectors:
- transmits communicable pathogens from one host to the other, usually animals
- different from transmission between animals and humans e.g. bird flu
23
Q
Factors that increase the probability of catching a communicable disease
A
- overcrowded living and working conditions
- poor nutrition
- compromised immune system
- climate change (can introduce new vectors)
- culture and infrastructure (traditional medicine can increase transmission)
- socioeconomic factors such as a lack of trained health professionals
24
Q
transmission of pathogens between plants
A
Direct transmission:
- direct contact of a healthy plant with any part of a diseased plant
Indirect transmission:
- soil contamination
- vectors (wind, water, animals, humans)
25
Factors affecting the transmission of communicable diseases in plants
- planting varieties of crops that are susceptible to disease
- over-crowding increases the likelihood of contact
- poor mineral nutrition reduces resistance of plants
- damp, warm conditions increase the survival and spread of pathogens and spores
- climate change - increased rainfall and wind promote the spread of diseases; changing conditions allow animal vectors to spread to new areas; drier conditions may reduce the spread of disease
26
The HIV cycle
- HIV virion glycoprotein binds to helper T cell receptor and fuses to cell surface membrane
- HIV RNA, reverse transcriptase, integrase and other viral proteins enter host cell (endocytosis)
- Viral DNA is formed by reverse transcriptase
- Viral DNA is transported across the nucleus and integrated into the host DNA by the enzyme integrase
- New viral RNA is used to make viral proteins
- New viral RNA and proteins move to surface and are assembled
- ‘Budding’ occurs as new virion fuses with cell membrane and is released
27
The malaria cycle
- Plasmodium protists in mosquito salivary glands
- Protists enter host when infected mosquito sucks blood
- Protists carried to liver by bloodstream and reproduce asexually
- Protists begin cycle of infecting RBCs, reproducing and bursting out
- Some cells develop into male and female gametes
- Gametes move into mosquito’s gut when it feeds on infected blood
- Fertilisation occurs and zygote then divides by mitosis
- New cells burst out of cells in gut and migrate to salivary glands
28
How do plants recognise an attack
- receptors in the cells respond to molecules from the pathogens or to chemicals produced when the plant cell wall is attacked
- this stimulates the release of signalling molecules that switch on genes in the nucleus
- defensive chemicals are produced, sending alarm signals to unaffected cells to trigger their defences
- polysaccharides (callose and lignin) are made to strengthen cell walls
29
Physical defences of plants - callose
- Polysaccharide callose (β-1,3 and β-1,6 linkages between glucose monomers) is synthesised
- Callose is deposited between cell walls and membranes in cells adjacent to those infected
- these callose papillae act as barriers, preventing pathogens entering cells around site of infection
- Callose continues to be deposited in large amounts
- Lignin is added, thickening and strengthening mechanical barrier
- Callose blocks sieve plates in the phloem, sealing off infected areas and preventing the spread of pathogens
- Callose is deposited in plasmodesmata between infected cells and neighbours, sealing them from healthy cells
30
Chemical defences of plants
- insect repellents (pine resin and citronella)
- insecticides (caffeine)
- antibacterial compounds including antibiotics (phenols = antiseptics)
- antifungal compounds (saponins interfere with fungal cell membranes - chitinases)
- anti-oomycetes (glucanases break down glucans in cell wall)
- general toxins (cyanide)
31
Non-specific animal defences for keeping pathogens out of the body
- the skin covers the body and also has a skin flora of healthy microorganisms that outcompete pathogens
- many body tracts are lined with mucous membranes that trap microorganisms are contain lysozymes and phagocytes
- lysozymes in tears, urine and stomach acid destroy bacteria and fungal cell walls
32
Blood clotting and wound repair
When platelets come into contact with collagen in the skin or the wall of a damaged blood vessel, it starts to secrete substances:
- thromboplastin, an enzyme that triggers a cascade of reactions resulting in a blood clot (thrombus)
- serotonin, which makes the smooth muscles in the walls of the blood vessels contract, so they narrow and reduce the supply of blood to the area
33
How does thromboplastin create a blood clot
- thromboplastin and calcium ions from plasma catalyses prothrombin into thrombin
- thrombin catalyses soluble fibrinogen into insoluble fibrin, which creates a clot/thrombus
34
What is the inflammatory response
- a localised response to pathogens (or damage and irritants) resulting in inflammation at the site of a wound
- inflammation is characterised by pain, heat, redness and swelling of tissue
35
How does the inflammatory response work
Mast cells are activated in damaged tissue and release the chemicals histamines and cytokines:
- histamines make the blood vessels dilate, causing localised heat and redness. The raised heat helps prevent pathogens from reproducing
- histamines also make blood vessel walls more leaky so blood plasma is forced out into tissue fluid, causing swelling (oedema) and pain
- cytokines attract phagocytes to the site to dispose of pathogens by phagocytosis
36
How does the inflammatory response work
Mast cells are activated in damaged tissue and release the chemicals histamines and cytokines:
- histamines make the blood vessels dilate, causing localised heat and redness. The raised heat helps prevent pathogens from reproducing
- histamines also make blood vessel walls more leaky so blood plasma is forced out into tissue fluid, causing swelling (oedema) and pain
- cytokines attract phagocytes to the site to dispose of pathogens by phagocytosis
37
Fevers
A non-specific defence if pathogens get into the body. Cytokines stimulate the hypothalamus so reset the thermostat, so the body temperature goes up
- higher temperatures inhibit pathogen production
- the specific immune system works faster at higher temperatures
38
Phagocytosis in macrophages
- pathogens produce chemicals that attract phagocytes
- phagocytes recognise the pathogen as non-self due to antigens and binds to it
- the phagocyte engulfs the pathogen and encloses it in a vacuole called a phagosome
- a lysosome combines with it, phagolysosome
- enzymes break down the pathogen
- digested pathogen absorbed by phagocyte
– antigens combine with MHC in the cytoplasm
- MHC/antigen complex is displayed on phagocyte membrane, making an antigen presenting cell
- APC stimulates other cells involved in the specific immune response
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Opsonins
Molecules produced by phagocytes that ‘tag’ pathogens making them more visible to other phagocytes, enhancing phagocytosis
40
Phagocytosis in neutrophils
- pathogens produce chemicals that attract phagocytes
- phagocytes recognise the pathogen as non-self due to antigens and binds to it
- the phagocyte engulfs the pathogen and encloses it in a vacuole called a phagosome
- a lysosome combines with it, phagolysosome
- enzymes break down the pathogen
- digested pathogen absorbed by phagocyte
41
Antigens
- all molecules have antigens on their surfaces
- the body recognises the difference between self antigens and non-self antigens
- non-self antigens trigger an immune response
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Antibodies
Y-shaped glycoproteins called immunoglobulins
- binds to a specific antigen on the pathogen or toxin
- forms an antigen-antibody complex
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The specific immune system
- targets a specific pathogen
- slower to respond than non-specific immune system
44
What are the two main responses involved in the specific immune system
- the cellular/cell-mediated response targets pathogens inside cells
- the humoral/antibody-mediated response targets pathogens in body fluids with antibodies
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How do antibodies defend the body
- acts as an opsonin so phagocytes can engulf the pathogen
- most pathogens can no longer invade cells
- act as agglutinins causing pathogens to clump together making it easier for phagocytes to engulf and prevents them spreading through the body
- can act as anti-toxins, binding to toxins produced by pathogens and making them harmless
46
Where do T lymphocytes mature
Thymus gland
47
Where do B lymphocytes mature
Bone marrow
48
T helper cells
- CD4 receptors on cell-surface bind to surface antigens on APCs
- Produce interleukins, a type of cytokine
that stimulate B cells to:
- increase antibody production
- produce other types of T cells
- attract and -stimulate macrophages
49
T killer cells
- Destroy pathogen carrying the antigen
- Produce chemical perforin
- Perforin kills pathogen by making holes in cell membrane so it is freely permeable
50
T memory cells
- Persist for a long time and are part of immunological memory
- On encountering antigen for a second time, divide rapidly to form huge number of clones of T killer cells that destroy the pathogen
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T regulator cells
- Suppress the immune system, acting to control and regulate it
- Stop the immune response once the pathogen is eliminated
- Ensure body recognises self antigens, preventing autoimmune response
Interleukins are important in this control
52
Plasma cells
(B lymphocyte)
- Produce antibodies to a particular antigen
- Release them into circulation
- Active plasma cells only persist for a few days
- Will produce ~2000 antibodies per second in this time
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B effector cells
Divide to form plasma cell clones
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B memory cells
- Persist for a long time and provide immunological memory
- Programmed to remember a specific antigen
- Enable body to make a very rapid response when a pathogen carrying that antigen is encountered again
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Cell-mediated immunity
- In the non-specific defence system, macrophages engulf and digest pathogens in phagocytosis
- They process antigens to form APCs
- Receptors on some T helper cells fit antigens
- T helper cells are activated and produce interleukins
- These stimulate more T cells to divide rapidly by mitosis
- Form clones of identical T helper cells carrying the correct antigen to bind to a particular pathogen
56
What do the cloned T-cells do in cell-mediated immunity
Either:
- develop into memory cells, which give a rapid response if this pathogen invades the body again
- produce interleukins which stimulate phagocytosis
- produce interleukins that stimulate B cells to divide
- stimulate the development of a clone of T killer cells that are specified and destroy infected cells
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Interleukins
A type of cytokine (cell signalling molecule)
58
What cells do T lymphocytes usually respond to in cell mediated immunity
- T lymphocytes respond to the cells of an organism that have been changed in some way
e.g. virus infection, antigen processing, or by mutation (e.g. cancer cells)
- Also respond to cells from transplanted tissue
- Cell-mediated response particularly important against viruses and early cancers
59
Humoral immunity
- Activated T helper cells bind to B cell APC. (Clonal selection – where B cell with correct antibody is selected for cloning)
- interleukins produced by activated T-helper cells activate B cells
- activated B cell divides by mitosis to gives clones of plasma and B memory cells (clonal expansion)
- cloned plasma cells produce antibodies that fit antigens on pathogen surface; binding and disabling them or acting as opsonins or agglutinins – primary immune response
- If the body is infected by same pathogen again, the B memory cells divide rapidly to form plasma cell clones, producing antibodies and destroying pathogen – secondary immune response
60
What are autoimmune diseases
When the immune system stops recognising 'self' cells and start to attack healthy body tissue
-in some cases it is because T regulator cells do not work efficiently, but could be genetic or post-viral
- can cause chronic inflammation or complete breakdown of healthy tissue
- immunosuppressant drugs can be used as treatment, but stops immune system working
61
Types of autoimmune diseases
Type 1 diabetes:
- affects the insulin secreting cells of the pancreas
- insulin injections, immunosuppressants, pancreas transplant
Rheumatoid arthritis:
- affect joints
- anti-inflammatory drugs, immunosuppressants, steroids, pain relief
Lupus:
- affects skin, joints, fatigue
- can attack any organ
- anti-inflammatory drugs, immunosuppressants, steroids
62
Natural active immunity
T and B memory cells staying in your body after you meet a pathogen for the first time means your immune system can recognise and destroy the same pathogen before it causes disease symptoms if it enters the body for a second time
63
Natural passive immunity
New born babies do not have a mature immune system, so don't produce antibodies in the first few months. Some antibodies are passed through the placenta. The first mammalian milk a mother makes is called colostrum and is very high in antibodies. A breast-fed baby will have the same level of antibody protection against disease as its mother, which is usually pathogens in its environment
64
Artificial active immunity
An immune system is stimulated to make its own antibodies and therefore memory cells to a safe form of an antigen in the form of a vaccine injected into the bloodstream
65
How are pathogens made safe in order to produce vaccines
- killed or inactivated bacteria or viruses such as whooping cough
- attenuated (weakened) strains of live bacteria or viruses such as rubella, polio
- toxin molecules that have been altered and detoxified such as tetanus
- isolated antigens extracted from the pathogen such as influenza
- genetically engineered antigens such as hepatitis B
66
Artificial passive immunity
Gives temporary but life saving immunity by injecting antibodies formed in another individual (often an animal). Can be used as treatment for people with tetanus or rabies
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Epidemic
when a communicable disease spreads rapidly to a lot of people at a local or national level
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Pandemic
When a disease spreads rapidly across a number of countries and continents
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Herd immunity
When a significant number of people have been vaccinated it gives protection to those who do not have immunity, so there is minimal opportunity for an outbreak to occur
70
What communicable diseases cannot be prevented by vaccinated
Malaria:
- protoctist hides inside erythrocytes
HIV:
- enters macrophages and T helper cells, so destroys immune system
71
local vaccination
vaccinating only the most at risk people e.g. by age group
72
Pros of vaccination
- Vaccines have helped to control lots of infectious disease e.g. measles, polio, whooping cough
- Highly effective e.g. polio infections have fallen by 99%
- Can lead to the eradication of a diseases e.g. smallpox
- More effective and cost-efficient than treatment
73
Cons of vaccination
- do not always provide immunity
- Some diseases require booster injections
- Can cause reactions, sometimes severe e.g. swelling, fever, seizures
- Not available to all population e.g. elderly, immunocompromised
74
Penicillin
- Antibiotic
- Commercial extraction originally from mould growing on melons
- Common antibiotic that kills bacteria by weakening cell walls
75
Digoxin
- Glycoside
- Isolated and purified from digitoxin, originally extracted from foxgloves
- Powerful heart drug used to treat atrial fibrillation and heart failure
76
Pharmacogenetics
the study of genetic variation that gives rise to differing responses to drugs
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Synthetic biology
- Using techniques of genetic engineering to develop bacteria populations that can produce much needed drugs
- nanotechnology
78
pharmacogenomics
the study of genes that code for enzymes that metabolize drugs, and the design of tailor-made drugs adapted to an individual's genetic make-up.
79
Development of antibiotic resistance
- Chance mutation in one bacterium produces a gene for antibiotic resistance
- Antibiotic applies a selection pressure
- bacteria without the resistance gene are killed
- Resistant bacteria survive and reproduce, increasing in number
- strong natural selection for bacteria with antibiotic-resistant gene
- Continued selection pressure means almost all of the population will be antibiotic-resistant
80
How can antibiotic-resistant infections be reduced?
- ensuring every course of antibiotics is completed to reduce risk of resistant individuals surviving
- good hygiene in hospitals, care homes and in general
- minimising use of antibiotics, don't use them for viruses or in agriculture
