communicable diseases 4.1 Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

Types of pathogens

A
  • bacteria
  • fungi
  • viruses
  • protictisa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

examples of bacterial diseases

A
  • tuberculosis (TB) in humans .Spread by the bacterium Mycobacterium tuberculosis (M. tuberculosis or Mycobacterium bovis (M.bovis).
    Spread through droplets of water in the air released through
    sneezing/coughing
    • This is then inhaled by an uninfected individual.
  • bacterial meningitis in humans. N. meningitidis causes symptoms such as fever, headache, neck stiffness and a characteristic rash.
  • Ring rot diseases in potato plants. The bacteria infect the vascular tissue and prevent the transport of water, causing the plant to wilt and die
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

examples of fungal diseases

A
  • Black Sigatoka in bananas. It spreads through the leaves of the plant, reducing its ability to photosynthesises. lack of photosynthesis causes parts of the leaf to die; producing black streaks. Eventually, the whole leaf dies
  • athletes foot- growth under skin of feet.
  • Ringworm (cattle)- growth of fungus in skin with spore cases through the skin to cause a rash
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

examples of viral diseases

A
  • viruses infect host cells and hijack their machinery to replicate their own genetic material and proteins.
  • Tobacco Mosaic Virus (TMV).causes a distinct yellowing of the leaves which produces a mosaic pattern
  • influenza attacks the respiratory system and causes muscle pains and headaches
  • HIV attacks cells in the immune system and compromises the immune response,

-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

examples of protistista diseases

A
  • can cause harm by entering host cells and feeding on the contents as they grow
    It is carried in the salivary glands
    • This mosquito then feeds on a human by biting them
    • Plasmodium parasite then passes from the saliva of the female mosquito Anopheles into the humans blood stream
    • Plasmodium infects the hepatoctes (liver cells) and ervthrocytes causing disruption to the blood flow to
    )
    vital organs
  • is transmitted via spores. The first signs of potato blight are small, dark brown marks on the leaves.
    The protist destroys potato and tomato crops leaving them completely inedible
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

direct transmission

A
  • direct physical contact e.g. touching a infected person or contaminated surface(including soil)
  • oral e.g. eating or drinking foods contaminated by the pathogens
  • droplets infection
  • through spores (very small reproductive structures that are released into the environment. They are dispersed via wind or water known as airborne transmission), to prevent this transmission wear mask and wash the skin after coming in contact with the soil.
  • social factors: overcrowding, poor ventilation, poor health,poor diet
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

indirect transmission

A

-pathogens are transmitted via a vector

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how does climate have an affect on transmission?

A

-many pathogens grow and reproduce more rapidly in warm and moist conditions therefore there is a greater variety of diseases to be found in warmer climates, and animals or plants living in these regions are more likely to become infected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

passive defences

A
  • defences present before infection, prevent entry and spread of the pathogens. Include physical barriers and chemical barriers.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

example of physical defences

A
  • cellulose cell walls- act as a barrier + contain a variety of chemical defences which are activated when the pathogen is detected
  • lignin - thickens the cell wall
  • waxy cuticle-prevents water collecting on the cell surfaces.so pathogens that collect in water will not be on the cell surface
  • bark-contain a variety of chemical defences
  • stomatal closure
  • callose- a large polysaccharide deposited around the sieve plates blocking the flow of the sieve tubes which prevents pathogens from spreading around the plant.
  • tylose formation- blocks the xylem vessels preventing the spread of pathogens. tylose also contains chemicals such as terpenes that are toxic to pathogens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

active defences

A
  • occurs when the chemicals such as proteins and glycolipids in the pathogens cell wall are detected by the plant cells. the plant responds by fortifying the defences already present.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

example of active defences

A
  • cell walls become thickened and strengthened with additional cellulose
  • deposition of callose between plant cell wall + membrane near the invading pathogen
  • an increase in production of chemicals
  • necrosis- few cells of the plant are sacrificed to save the rest of the plant.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

chemical defences examples

A
  • tannins- create a bitter taste, found in the bark
  • insect repellent
  • alkaloids- nitrogen-containing compounds such as caffeine, nicotine, cocaine and morphine give a biter taste to inhibit herbivores feeding.
  • hydrolytic enzymes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

primary non-specific defences against pathogen in animals (6)

A
  • skin acts as a physical barrier to pathogens.
  • mucus membrane. goblet cells produced mucus trapping pathogens which the cilla wafts away.
  • When a pathogen irritates the lining of an airway it can trigger an expulsive reflex; a cough or sneeze which result in a sudden expulsion of air containing the pathogen.
  • lysosomes. breakdown the cell wall of bacteria + hydrochloric acid
  • blooding clotting- dries to form a scab which prevents bleeding
  • inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

describe inflammation

A
  • pathogen is detected by mass cells which realises histamines and cytokines
  • histamines causes the blood vessels to dilate therefore the blood vessel walls become more permeable. blood plasma and white blood cells leave the blood and enter the tissue fluid increasing tissue fluid, which causes swelling(oedema). other symptoms are swelling + localised heat inhibiting pathogen reproduction. more white blood cells in the tissue fluid near the cells can tackle the pathogen.
  • more fluid enters the lymphatic system
  • mass cells allow release cytokines for cell signalling which attract phagocytes for increased phagocytosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are phagocytes?

A

-white blood cells that are produced continuously in the bone marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

3 types of phagocytes

A
  • neutrophils
  • macrophages
  • dendritic cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

describe the process of phagocytosis

A
  • the receptor on the phagocyte recognises the antigen on the pathogen as foreign
  • the phagocyte engulfs the pathogen(endocytosis) forming a phagosome
  • lysosomes contain in the phagocyte fuse with the phagosome
  • the lysosomes then digest the pathogen within
  • phagocyte dies and may collect in an area of infection to form pus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

describe phagocytosis with a macrophage

A
  • (same stages as normal phagocytosis)
  • instead the lysosomes digest everything except for there antigen
  • the pathogens antigen is displayed on the surface of the macrophage (through a structure called the major histocompatibility complex)
  • the macrophage becomes a antigen-presenting cell
  • the displayed antigens can then be recognised by lymphocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

difference between neutrophils and macrophages

A
  • Macrophages are larger
  • macrophages are longed-lived cells as after phagocytosis it migrates to the lymph node whereas neutrophils have a long life span
  • macrophages rather than remaining in the blood, they move into organs whereas neutrophils remain in the blood
  • After being produced in the bone marrow, macrophages travel in the blood as monocytes, which then develop into macrophages once they leave the blood to settle in the various organs
  • neutrophils have a multilobed nucleus whereas monocytes have a large kidney-shaped nucleus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

t lymphocytes

A
  • made in the bone marrow, but mature in the thymus

- differentiate/develop into T helper cells, T killer cells, T regulator cells and T memory cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

T helper cells

A
  • CD4 receptors on the cells surface membrane binds to the antigen + MTH complex on the AP
  • detection of the MHC complex lets the cell know that this is an APC. not a pathogen to be destroyed
  • the cell releases interleukins which stimulates B cells to make antibodies, other T cells to divide ,macrophages to enhance phagocytosis
23
Q

T killer cells

A
  • It attaches to the foreign antigens on the cell surface membranes
  • destroys host cells by releasing perforins which makes holes in the cells surface membrane allowing toxins to enter killing the cell and the pathogens inside them
24
Q

T regulator cells

A
  • suppress the immune response after the pathogen has been successfully destroyed.
  • involved in preventing autoimmunity
25
Q

T memory cells

A
  • provides immunological memory of the antigen

- recognises the foreign antigen to rapidly produce secondary response providing long-term immunity.

26
Q

describe the cell-mediated immunity response (action of T lymphocytes)

A
  • phagocytosis occurs and the cell becomes antigen presenting.
  • T helper cells with the receptor complementary to the antigen on the APC binds (clonal selection)
  • the T helper cell releases interleukins altering other cells
  • this stimulates other T cells to divide rapidly by mitosis to form a clone (clonal expansion)
  • clones develop to become T memory cells killer cells, stimulates phagocytosis or stimulates B cells to divide
27
Q

B lymphocytes

A
  • made and mature in the bone marrow

- differentiate into plasma cells and B memory cells.

28
Q

humoral immunity

A
  • B cells undergo phagocytosis becoming B antigen- presenting cells
    -T-helper cells receptor binds to the complementary antigen on the B cell and release interleukins activating them (clonal selection)
    -The B cells are now activated to divide by mitosis to give a clone (clonal expansion) which differentiate into plasma cells.
  • The cloned plasma cells produce antibodies that exactly fit the antigens on the
    pathogens surface
    -The antibodies attach to antigens on the pathogens and destroy them. This is
    the primary immune response.
  • Some B cells develop into memory cells
29
Q

3 main group of antibodies

A
  • opsonin’s- bind to the antigens on the pathogen acting as a binding site for phagocytic cells, so these can more easily bind and destroy the pathogen, -Increases the changes of phagocytosis
  • agglutinins- antibodies have two binding site so can bind to the antigens on to pathogens at the same time causing the pathogens to become clumped together. The pathogens are too large to enter the host cell and increases the likelihood of phagocytosis
  • antitoxins-forms a antibody-toxin complex neutralising the toxin
30
Q

structure of antibodies

A
  • Y shaped consists of 4 polypeptide chains 2 light,2 heavy
  • disulphide bridges hold the polypeptide chains together
  • variable region- complementary shape to the antigen on the pathogen
  • constant region-same in a all antibodies, may have a site for easy binding of phagotic cells
  • hinge region- allows flexibility so molecules can bind more than one antigen
31
Q

describe why the secondary response is faster and stronger than the primary response

A
  • the pathogen enters the body for the second time therefore the B and T memory cells recognise the antigen on the pathogen so clonal selection is faster and clonal expansion. memory B lymphocytes is activated and produce plasma cells which differentiate into the correct antibodies and a higher concentration T memory cells are activate and differentiate into to the correct type of T lymphocytes to destroy the pathogen
  • the secondary response get rid of the pathogen before you begin to show symptoms,
32
Q

differences between active and passive immunity

A
  • active immunity is when your immune system produces its own antibodies after being stimulated by a pathogens antibody. passive immunity is when you are given antibodies from a different organism. no memory cells are produced
33
Q

active natural

A
  • when you become immune after catching a disease
34
Q

artificial active

A

-you become immune after being given a vaccination

35
Q

passive natural

A
  • when a baby becomes immune due to antibodies it receives from its mother, though the placenta and breast milk
36
Q

Passive artificial

A
  • when you become immune after being injected with antibodies from someone else
37
Q

autoimmune disease

A

-an abnormal immune response against tissues normally in the body
-e.g. lupus- caused by the immune system attacking cells in the connective tissues
-rheumatoid arthritis -when the immune system attacks cells in the joints
both causes painful inflammation
-diabetes type I body cells attack B cells

38
Q

routine vaccines

A
  • the MMR- protects against measles, mumps and rubella. given to children around a year old and again before they start school
  • the Meningitis C vaccine- protects again meningitis. first given as an injection to babies at 3 months. booster are given to 1 year olds and teenagers
39
Q

vaccination programmes

A
  • the influenza flu vaccine changes every year, because the antigen on the surface of the influenza virus changes regularly, producing a new strain so vaccination are given every year to those at risk so they can gain immunity.
40
Q

antiobiotic resistance

A
  • there is genetic variation in the population of bacteria
  • antibiotic is the selection pressure
  • the more resistant strains survive and reproduce passing on the resistant alleles
  • overtime the population of bacteria becomes resistant
  • the antibiotic becomes ineffective
41
Q

examples of antibiotic resistant bacteria

A
  • MRSA and clostridium difficile
42
Q

possible sources of medicine

A

-plants, animals or microorganisms e.g. penicillin is obtained from fungus

43
Q

personalised medicines

A
  • peoples bodies respond to drugs in different ways making some drugs more effective for some, personalised medicine is medicines tailored to an individual’s DNA. so that a person is prescribed the most effective dug to them.
44
Q

synthetic biology

A

-using technology to design and make artificial proteins ,cells or even microorganisms,

45
Q

B memory cells

A
  • immunological memory of antigen to provide a rapid secondary response
46
Q

Health

A
  • free from disease
  • physical and mental and social well-being
47
Q

What is a parasite

A
  • an organism that lives in host harming them and feeds on the host taking nutients
48
Q

Lymphatic system

A

-excess tissue fluid is drained into the lymphatic system
-pathogen will nester the lymph
- transport the lymph nodes
-lymph nodes swell to produce phagocytes and lymphocytes

49
Q

Monocyte blood smear

A

-unilobular nuclei

50
Q

Immune response

A

-response to an antigen
-involves lymphocytes/ production of antibodies

51
Q

Vaccinations

A
  • dead or weakened pathogen
  • creates herd immunity =
    High percentage of people with vaccine
  • ring vaccine = the most vulnerable are protected
52
Q

Why is it beneficial to vaccinate the population

A
  • so there is little impact on the economy as people can work and it’s cheaper to prevent disease than treat an ill person
    M
53
Q

Groups of people vulnerable to diseases

A
  • pregnant women as the foetus has a weak immune system
    -elderly people
  • people with HIV
  • babies
    -people on chemotherapy