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SNAB biology hoe > 6B Microorganisms and Immunity > Flashcards

6B Microorganisms and Immunity Flashcards

1
Q

immune system

A

biological processes that identify and kill pathogens

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2
Q

phagocytosis

A

engulfment and digestion of pathogens by w.b.c

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3
Q

bone marrow

A

site of B cell maturation

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4
Q

mast cells

A

immune system cells -> release histamine

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5
Q

T helper cells

A

release substances to activate …

  • B cells
  • T killer cells
  • macrophages
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6
Q

Tuberculosis

A
  • infectious disease of respiratory system
  • caused by Mycobacterium TB
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7
Q

HIV

A

virus causing AIDS -> infects and destroys T helper cells (host cell)

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8
Q

AIDS

A
  • disease of human immune system
  • increases chance of other diseases (infections, cancer)
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9
Q

immunity

A

having sufficient B and T memory cells to avoid disease

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10
Q

booster injections

A

re-exposure to antigen

  • increases no. B and T memory cells to maintain protective levels so more antibodies
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11
Q

herd immunity

A

when high enough proportion of pop is vaccinated that those without immunity are PROTECTED

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12
Q

bacteriCIDAL

A

antibiotics that destroy bacteria

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13
Q

bacterioSTATIC

A

antibiotics that prevent MULTIPLICATION OF BACTERIA

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14
Q

antigenic drift

A

changes in antigens due to mutations in pathogen

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15
Q

what is the name of the markers on microorganisms that allow cell-to-cell recognition?

A

antigens

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16
Q

self antigens

A

produced by own body

DON’T STIMULATE IMMUNE RESPONSE

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17
Q

what happens after pathogens are engulfed by phagocytosis?

check if right

A
  • phagocytes transfer antigens of digested pathogen to cell surface membrane
  • they become antigen presenting cells eg. MACROPHAGES
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18
Q

what do antigen presenting cells
(eg. macrophages) do?

A

activate specific immune response

-> occurs when lymphocytes bind to presented antigens

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19
Q

macrophage

A

type of phagocytic w.b.c

long lived

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20
Q

bacteria

A
  • single-celled
  • prokaryotic
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21
Q

pathogen

A

organism that causes disease

diseases caused by pathogens = infectious

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22
Q

describe how HIV affects immune system

what does it mean 2 RNA strands????

A

HIV replicates inside host T helper cell

  1. attachment protein attaches to CD4 receptor on cell membrane of T helper cell
  2. capsid released into cell -> uncoats and releases RNA into cell’s cytoplasm
  3. inside cell: REVERSE TRANSCRIPTASE used to make COMPLEMENTARY STRAND of DNA from viral RNA template
  4. from this, DOUBLE STRANDED DNA made and INSERTED into human DNA
  5. viral proteins assembled into new viruses -> bud from cell and go to infect other cells
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23
Q

inflammation

A

site where pathogen enters body

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24
Q

describe inflammation process

A
  1. immune system cells recognise foreign antigens on surface of pathogen and release HISTAMINE THAT TRIGGERS INFLAMMATION
  2. histamine causes VASODILATION (widening of ARTERIOLES) around site -> increases blood flow to it
  3. molecules also increase PERMEABILITY OF CAPILLARIES
  4. -> increased blood flow = brings loads of immune system cells to site-> increased permeability = allows cells to move OUT OF BLOOD->INFECTED TISSUE
  5. immune system cells start to destroy pathogen
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25
Q

what are the body’s barriers to prevent infection?

A
  • STOMACH ACID -> acidic conditions (low pH) kill pathogens
    BUT some may survive and pass into small intestine where they invade cells of gut wall (eg cholera)
  • GUT AND SKIN FLORA -> billions of harmless microorganisms -> compete with pathogens for nutrients and space -> harder for pathogens to infect body
  • LYSOZYME -> mucosal surfaces (eyes, mouth, nose) produce secretions (tears, saliva, mucus) -> contain enzyme lysozyme -> kills bacteria by damaging cells walls -> makes bacteria burst open (lyse)
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26
Q

what are initial symptoms of AIDS?

A
  • minor infections of mucous membranes (inside of nose, ears, genitals)
  • recurring respiratory infections -> caused by lower than normal no. of T helper cells
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27
Q

symptoms of AIDS later on?

A
  • as AIDS progresses = less and less T helper cells
  • patients become prone to more serious infections eg. chronic diarrhoea and TB
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28
Q

passive immunity

A

acquired without an immune response

antibodies gained are from another source e NOT OWN BODY

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29
Q

artificial passive immunity

A

injection / transfusion of antibodies e.g. the tetanus antitoxin

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30
Q

artificial active immunity

A

vaccination

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31
Q

natural active immunity

A

exposure to a pathogen

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32
Q

natural passive immunity

A

antibodies received from another organism eg. from placenta or breastmilk

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33
Q

role of T helper cells in developing immunity after a vaccine

A
  • T helper cells BIND to APC
  • leads to production of ACTIVE T- helper cells
  • T helper cells activate B cells to become PLASMA CELLS
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34
Q

specific immune response

secondary response

A

DELAYED response directed at SPECIFIC pathogen

35
Q

non-specific immune response

primary response

A

IMMEDIATE response directed at ALL pathogens

36
Q

suggest how antihistamines work

A

bind to histamine receptors and BLOCK histamine from binding

37
Q

explain why someones wound may become hot, red and swollen

A

hot -> increase in metabolic rate and lots of cells RESPIRING

red -> increased blood flow

swollen -> leakage of fluid from CAPILLARIES

38
Q

interferons

A
  • anti viral proteins
  • made by cells when infected with virus
  • prevent virus spreading to uninfected cells
39
Q

how do interferons prevent virus from spreading to uninfected cells?

A
  • stop production of viral proteins
  • ACTIVATE CELLS involved in SPECIFIC IMMUNE RESPONSE to kill infected cells
  • activate mechanisms of non-specific immune response
    eg. PROMOTE INFLAMMATION by bringing immune system cells to site of infection
40
Q

2 main types of lymphocytes

A
  • B cells
  • T cells
41
Q

neutrophils

A

type of phagocyte

short lived

42
Q

lysosomes

A

membrane organelles

contain digestive enzymes called lysozymes -> digest unwanted material present in cells

43
Q

pus is a sign of what?

A

dead neutrophils

44
Q

B cells divide to produce two clones of cells …

A
  • B effector cells
  • B memory cells
45
Q

B effector cells

A

differentiate into plasma cells* and release ANTIBODIES into blood and lymph in response to antigen

short lived, last a few days

*they specialise to become plasma cells -> plasma = B effector

46
Q

B memory cells

A

remain in body for years

enable organism to respond quicker to same antigen in future

47
Q

cell clonal selection

A

process of B cell division

48
Q

antibodies

A
  • secreted by plasma cells
  • bind to specific antigens identifying them for easier destruction
  • and agglutinating them so phagocytosis is quicker
49
Q

granuloma

A

anaerobic masses of tissue containing dead bacteria and macrophages

50
Q

T cells

A

immature T cells leave bone marrow to mature in thymus

mature T cells have specific cell surface receptors
(T cell receptors) -> similar structure to antibodies and are each SPECIFIC TO ONE ANTIGEN

51
Q

T killer cells

A

bind to antigens and destroy their infected cells

52
Q

T memory cells

A

remain in blood
-> enable faster specific immune response if same pathogen encountered again in future

53
Q

what role to cytokines play in making sure there are enough
T killer cells?

is this answer right???

A

stimulate differentiation of T cells

54
Q

(compare and contrast B and T cells)

check if this is right

A
  • both are WBCs
  • B cells mature in bone marrow and T cells mature in thymus
  • B cells respond to foreign cells OUTSIDE BODY CELLS, bacteria, virus whereas T cells respond to foreign material INSIDE BODY CELLS
55
Q

compare and contrast bacteria and viruses

A
  • both have nucleic acids (DNA or RNA in viruses and only DNA in bacteria)
  • bacteria are small prokaryotes whereas viruses are not cells
    -> just particles
  • bacteria may have plasmids whereas viruses do not have them
  • bacterial DNA is double stranded whereas viral (DNA / RNA) is single / double stranded
56
Q

what are the 4 entry points for pathogens?

A
  • broken skin -> access to tissues and bloodstream
  • dig system -> contaminated food / drink
  • respiratory system -> inhaling
  • mucosal systems eg. inside of nose, mouth, genitals
57
Q

histamine

A

chemical signalling molecule that enables cell signalling / communication between cells

stimulates:

  • vasodilation
  • leaky capillary walls
  • phagocytosis
58
Q

what does the non-specific immune response include?

happens first!!

A
  • inflammation
  • interferon production -> prevents virus spreading to uninfected cells
  • phagocytosis -> WBCs engulf pathogens
  • lysozyme action -> kills bacteria cells by damaging cell wall
59
Q

describe the process of phagocytosis

A
  1. phagocyte recognises antigen on pathogen
  2. engulfs pathogen
  3. pathogen contained in phagocytic vacuole
  4. lysosome fuses with phagocytic vacuole …
  5. … and lysozymes break down pathogen
  6. phagocyte presents antigen to activate other immune system cells - now an APC
60
Q

what does the specific immune response include?

A
  • phagocytes activate T cells
  • T helper cells activate B cells
61
Q

what are cytokines?

A

chemicals that T helper cells release

to stimulate ÷ and differentiation of B cells

62
Q

describe the process of activation of T helper cells

is this exactly what i need to know?

A
  1. bacterium engulfed by macrophage
  2. macrophage presents antigens -> becomes APC
  3. APC binds to T helper cell with complementary CD4 receptors
  4. T helper cell is activated and divides via mitosis to form …
  5. -> T memory cells
    -> active T helper cells
63
Q

compare and contrast the humoral response and the cell mediated response

check if right

A
  • humoral response produces antibodies whereas the cell mediated response produces T killer cells
  • cell mediated works against intracellular pathogens while humoral works against extracellular pathogens
  • both are specific to an antigen
  • both require formation of APCs and presence of MHCs
64
Q

explain why a person newly infected with TB may not show any symptoms

A

immune system ‘seals off’ infected phagocyte in structures (in lungs) called tubercles

-> bacteria become dormant in there so person shows no symptoms

65
Q

describe how Mycobacterium tuberculosis causes TB

A
  1. infection occurs when tiny droplets (cough / sneeze) containing bacteria inhaled
  2. in lungs, bacteria taken up by phagocyte -> survives and replicates inside phagocyte
  3. immune system seals off infected phagocyte using tubercles => bacteria now dormant
  4. later, dormant bacteria may become reactivated and overcome immune system -> likely in ppl with weak immune system eg. AIDS patients
  5. length of time between infection and development of TB varies (weeks to years)

M. tuberculosis has waxy cell wall-> so not killed by immune system

66
Q

explain the role of APCs

just ask about this whole card -> is it right??

A
  • macrophage displays antigen from pathogen on surface (after hydrolysis in phagocytosis)
  • enhances recognition in T helper cells which cannot directly interface with pathogens in body fluid

check

67
Q

name the 2 types of specific immune response

A
  • humoral
  • cell mediated
68
Q

how do antibodies help to clear an infection?

A
  • agglutinating pathogens so phagocytosis enhanced
  • neutralising toxins
  • preventing pathogens binding to human cells
    -> antibodies bind to antigens on pathogen, blocking receptors needed to bind to host cell
69
Q

differences between structure of membrane-bound and secreted antibodies

A

membrane bound have extra section of protein on heavy chain that anchors them to B cell membrane

70
Q

membrane bound antibody

A

attached to membrane of B cell

71
Q

secreted antibody

A

free from attachment

72
Q

why is non-specific / primary response slow?

A

aren’t many B cells that make antibody needed to bind to antigen

73
Q

HIV evasion mechanisms

A
  • high rate of mutation
  • mutations change antigen structures -> forming new strains of virus (a.k.a antigenic variation)
  • memory cells won’t recognise new strains
  • disrupts antigen presentation in infected cells -> prevents immune system recognising + killing them
74
Q

why are infections caused by antibiotic-resistant bacteria more common in hospitals?

A
  • more antibiotics used there
  • so bacteria in hospitals more likely to have evolved resistance against them
75
Q

how do hospitals prevent and control HAIs caused by antibiotic-resistant bacteria?

A
  • doctors shouldn’t prescribe antibiotics for minor bacterial / viral infections OR to prevent infections
  • doctors should use narrow-spectrum antibiotics if possible eg. when strain of bacteria person is infected with is identified
  • doctors should rotate use of diff antibiotics
  • patients should take all antibiotics prescribed so infection fully cleared
76
Q

describe what ribsosomes do in bacterial cells

A

produce proteins from mRNA

77
Q

devise an experiment to determine the effect of diff antibiotics on bacteria

A
  1. use sterile forceps to place mast ring (5+ diff a.b) OR paper discs soaked in distilled H₂O(-ve control) onto 2 diff petri dishes (where agar seeded with E.coli bacteria, spread evenly)
  2. close dishes and seal BUT leave small gap so O₂ can enter = no buildup anaerobic bacteria
  3. leave cultures to incubate at 25℃ for 24hrs
  4. open petri dish + use ruler to measure clear zone for each paper disc/ mast ring section (for diff a.b) -> use ∏r²

NOTES:
- aseptic tech throughout
- controls:
-> same conc a.b used
-> type and vol bacteria (E.coli)

78
Q

Mycobacterium tuberculosis evasion mechanisms

A
  • produce substances that prevent lysosome fusing with phagocytic vacuole …
  • so bacteria not broken down = multiply undetected inside phagocytes
  • disrupts antigen presentation -> prevents immune system recognising + killing infected cells
79
Q

introns

A

sections of gene that don’t code for a.a

80
Q

exons

A

sections of gene that do code for a.a

81
Q

explain how one gene can give rise to more than one protein through post-transcriptional changes to mRNA

(4 marks)

A
  1. during transcription, introns + exons copied into mRNA -> mRNA strands containing both introns + exons = pre-mRNA
  2. introns removed by “splicing” -> + exons joined, forming mRNA strands (takes place in nucleus -> is a post-transcriptional change)
  3. smt certain exons + introns removed = alt. splicing -> forms diff mRNA strands
  4. so more than 1 a.a seq = more than 1 protein produced from 1 gene
82
Q

describe some codes of practice hospitals use to prevent and control HAIs

A
  • staff + visitors wash hands before + after seeing patient
  • equipment/surfaces disinfected + sterilised
  • ppl with HAIs moved to isolation ward -> less liekly to transmit infection to other patients
83
Q

HIV requires a host cell to replicate.
suggest why it needs a host cell

A

doesn’t have stuff eg. enzymes + ribosomes to replicate on its own

SNAB biology hoe (15 decks)

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