Chapter 12- Communicable diseases Flashcards

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1
Q

2 main ways which pathogens work

A

damaging host tissues directly, producing toxins

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2
Q

classes of basic bacteria shapes

A

spirachaetes (corkscrew), spitilla (spiraled), vibrios(comma shaped), bacilli (rod shaped), cocci(spherical)

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3
Q

what are bacteriophages?

A

Viruses that attack bacteria and take over bacteria cells to reproduce. Can be used to identify and treat some diseases. They are important in scientific research.

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4
Q

what are pathogenic protists?

A

They need a vector to be transferred

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5
Q

what is tuberculosis caused by?

A

caused by the mycobacterium tuberculosis and m.bovis

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6
Q

plant physical defense

A
  1. Some molecules of the pathogen are recognised directly by the plant cell.
  2. When pathogen enzymes break down cell wall, the breakdown products are recognised.
  3. Signalling molecules alert nucleus to attack
  4. Polysaccharides (callose and lignin) are made to strengthen cell walls.
  5. Defensive chemicals give the alarm to other cells before they are affected.
  6. Some defensive molecules directly attack the pathogen.
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7
Q

Callose response

A
  1. When attacked plants produce high levels of a polysaccharide called callose which contains beta1-3 linkages and beta 1-6 linkages.
  2. beta 1-3 is oil like and helps maintain elasticity and tensile strength in cell walls. beta 1-6 connects components of the cell wall.
  3. Callose is synthesised and deposited between walls and membrane neighboring infected cells.
  4. Callose papillae act qas barriers preventing pathogens from accessing healthy cells.
  5. Ligin is added to increase strength of the mechanical barrier.
  6. Callose blocks sieve plates in phloem which prevents movement.
  7. Callose is then deposited in plasmodestama between injected cells and healthy cells
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8
Q

Barriers to pathogen entry in animals

A

mucous membrane- line pathways and airways in the body
skin- contains skin flora which competes with microorganisms for space
other- lysozome in tears and acid in the stomach

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9
Q

What is thromboplastin?

A

An enzyme which triggers reactions that cause blood clot.

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10
Q

What is serotonin?

A

Makes smooth muscle in blood vessels contract, so they narrow and reduce blood supply to the area.

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11
Q

What are histamines?

A

Cause blood vessels to dialate
Cause heat and redness
Raised temperature prevents pathogens reproducing
Makes vessels ‘leaky’ so more tissue fluid is forced out causing swelling and pain

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12
Q

What are cytokines?

A

Attract white blood cells to the site of infection
Dispose of pathogens by phagocytosis
Stimulate hypothalamus to increase body temperature to inhibit pathogen reproduction

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13
Q

What are the stages of phagocytosis?

A
  1. Pathogens produce chemicals that attract phagocytes
  2. Phagocytes recognise a non self protein on the pathogen
  3. The phagocyte engulfs the pathogen and encloses it in a vacuole called the phagosome
  4. The phagosome combines with the lysozome to form the phagolysozome
  5. The digested pathogen combines with the major histocompatability complex (MHC) in the cyptoplasm
  6. The MHC on the phagocyte membrane forms an antigen presenting cell (memory cell)
  7. This happens in the space of 10 minutes
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14
Q

What are opsonins and the two most effective examples?

A

Bind to pathogens and ‘tag’ them so they are easily recognised by phagocytes
The most effective are: antibodies immunoglobin G (IgG) and immunoglobin M (IgM)

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15
Q

How do antibodies work?

A

1- The antibody from the antigen antibody complex acts as an opsonin so that the complex is easily engulfed and digested
2- The pathogen can no longer effectively invade a cell
3- Antigens act as agglutinins which cause pathogens carrying the antigen-antibody complex to clump together
4- Due to this, phagocytosis happens at a faster and larger rate
5- Antibodies can act as anti-toxins building to the toxins produced by pathogens making them harmless

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16
Q

What are the different kinds of T-lymphocytes and their functions?

A

T-helper cells- Produce interleukins which stimulate B cells effectively, increase antibody production, produce T-helper cells and attract macrophages which ingest the pathogen
T-killer cells- Produce perforin which kills the pathogen by making holes in its cell membrane
T-memory cells- Part of immunological memory and during reinfection they release clones of T-killer cells to kill pathogen
T-regulator cell- regulate immune response and enables memorise pathogens and respond rapidly without causing autoimmune responseas

17
Q

What are the different types of B-lymphocytes?

A

Plasma cells- Produce antibodies, release into circulation, short life span and produce 2000 antibodies in lifetime
B-effector cells- Divide to form plasma cells clones
B-memory cells- Provide immunological memory and programmed to remember specific antigens to enable body to make a rapid response during re-infection

18
Q

What are the steps of cell mediated immunity?

A

1- Pathogen is engulfed and partially digested by the macrophage which creates an antigen presenting cell
2- The receptors on some T-helper cells fit the antigens- some T-helper cells produce interleukins which stimulate mitosis and clones help carry pathogen
3- Cloned T-cells may develop into T-memory cells, produce interleukins to stimulate phagocytosis, produce interleukins which stimulate B-cell division and stimulate development of T-killer cells

19
Q

What are the steps of humoral immunity?

A

1- Activated T-helper cells bind to the B-cell APC
2- Interleukins are produced by activated T-helper cells and help to activate B-cells
3- Activated B-cells divide (mitosis) to give clones of plasma cells and B-memory cells
4- Primary immune response- Cloned plasma cells produce antibodies that bind to antigens on surface of pathogen which plasma cells disables or act as opsonin’s or agglutinin’s
5- Secondary immune response- Some clones B-cells become B-memory cells ready to fight the 2nd round of pathogens

20
Q

What are the 5 things that vaccines contain?

A
Killed/ inactive bacteria
Attenuated strains of bacteria/ viruses
Detoxified or altered toxin molecules 
Isolated antigens extracted from pathogens 
Genetically engineered antigens
21
Q

What are the main 4 ways for developing drugs?

A

Identifying molecules made by organisms
Studying the genome to find suitable genes that code for potential drugs
Modifying drugs that already exist
Identifying molecules that fit into receptors/hormones/neurotransmitters and synapses

22
Q

What are the types of antibiotics?

A

Polymyxins- makes holes in cell membrane
Penicillin and cephalosporins- weaken cell wall
Sulfonamides- interfere with metabolic reaction
Tetracyclines and streptomycins- inhibit protein synthesis

23
Q

What is selective toxicity?

A

Can interfere with bacteria without affecting the metabolism of human cells

24
Q

What are the steps of antibiotic resistance?

A

1- A type of bacteria will be treated with an antibiotic and most of the bacteria will be destroyed
2- Some of the bacteria will have random genetic mutations which make them resistant to antibiotics
3- These will survive and reproduce until there is a new antibiotic- resistant strain of bacterium

25
Q

What is MRSA?

A

Bacterium carried by up to 30% of the population of skin and in their nose
Can cause boils, abscesses and septicaemia
Was treated effectively with methicillin (penicillin like antibiotic) but a mutation has produced resistant strains

26
Q

What is C.difficile?

A

Bacterium in the gut of approximately 5% of the population which produces toxins that damage the lining of the intestines leading to diarrhoea, bleeding and even death