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Biology Mock AS 2 > Microorganisms and Immunity > Flashcards

Microorganisms and Immunity Flashcards

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1
Q

how do prokaryotes differ from eukaryotes

A

A cytoplasm that lacks membrane-bound organelles

Ribosomes that are smaller (70 S) than those found in eukaryotic cells (80 S)

No nucleus, instead having a single circular bacterial chromosome that is free in the cytoplasm

A cell wall that contains the glycoprotein murein / peptidoglycan

cell membrane that contains folds known as mesosomes

Loops of DNA known as plasmids

Capsules

Flagella

Pili

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2
Q

what does a capsules / slime capsule do

A

protect bacteria from drying out and from attack by cells of the immune system of the host organism

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3
Q

what does flagella do

A

Long, tail-like structures that rotate, enabling the prokaryote to move

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4
Q

what does Pili do

A

Thread-like structures on the surface of some bacteria that enable the bacteria to attach to other cells or surfaces

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5
Q

describe the structure of a virus

A

A nucleic acid core
Their genomes are either DNA or RNA, and can be single or double-stranded

A protein coat called a ‘capsid’

do not possess a plasma membrane, cytoplasm, or ribosomes

an outer layer called an envelope formed from the membrane-phospholipids of the cell they were made in

contain attachment proteins that sticks out from the capsid or envelope
This enables the virus to attach itself to a host cell

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6
Q

structure of HIV

A

contains RNA and is a retrovirus

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7
Q

what is a helper T cell

A

a type of white blood cell that is normally responsible for activating antibody-producing B cells

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8
Q

how is HIV replicated

A

enters the helper T cells by attaching to a receptor molecule on the host cell membrane

The capsid enters the helper T cell and releases the RNA

The viral RNA is used as a template by reverse transcriptase enzymes to produce a complementary strand of DNA

Once this single-stranded DNA molecule is turned into a double-stranded molecule it can be successfully inserted into the host DNA

uses the host cell’s enzymes to produce more viral components which are assembled to form new viruses

enter the blood, where they can infect other helper T cells repeat the process

individual is HIV positive and may experience flu-like symptoms

individual enters the latency period after replication rate drops

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9
Q

what happens when virus reduces the number of helper T cells

A

B cells are no longer activated
No antibodies are produced

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10
Q

What are the four ways pathogens enter body

A

Broken skin

digestive system

respiratory system

Mucosal surfaces

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11
Q

what are the four barriers to infections

A

skin : blood clotting mechanism of the body plays an important role in preventing pathogen entry in the case of damage to the skin

microorganisms of the gut and skin: gut or skin flora they compete with pathogens for resources, thereby limiting their numbers and therefore their ability to infect the body

stomach acid : HCl creates an acidic environment that is unfavourable to many pathogens

lysozyme : damage bacterial cell walls, causing them to burst, or lyse

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12
Q

what is a specific response

A

response specific to a particular pathogen

recognise specific pathogens due to the presence of antigens on their cell surface

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13
Q

what is an antigen

A

molecules such as proteins or glycoproteins located on the surface of cells; their role is to act as an ID tag, identifying a cell as being ‘self’ or ‘non-self’

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14
Q

what is included in a non-specific immune response

A

Inflammation
Interferons
Phagocytosis

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15
Q

explain inflammation

A

surrounding area of a wound can sometimes become swollen

mast cells respond to tissue damage by secreting the molecule histamine
Histamine is a chemical signalling molecule that enables cell signalling

Histamine stimulates
Vasodilation increases blood flow through capillaries
Capillary walls more permeable

Phagocytes leave the blood and enter the tissue to engulf foreign particles

Cells release cytokines, another cell signalling molecule that triggers an immune response in the infected area

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16
Q

explain interferons

A

Cells infected by viruses produce anti-viral proteins called interferons which prevent viruses from spreading

inhibit the production of viral proteins, preventing the virus from replicating
They activate white blood cells involved with the specific immune response to destroy infected cells
They increase the non-specific immune response e.g. by promoting inflammation

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17
Q

explain phagocytosis

A

idea of binding of {bacteria / virus / pathogen / microorganism / antigen / non-self / foreign matter / eq} to (phagocytic) cell;

idea that {bacteria / virus / pathogen / microorganism / antigen / eq} is {engulfed by / taken into / endocytosis into
} (phagocytic) cell;

idea of bacteria being inside a {vacuole / phagosome /

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18
Q

mode of action of phagocytosis

A

Chemicals released by pathogens, as well as chemicals released by the body cells under attack. Histamine, attract phagocytes to the site where the pathogens are located

Phagocytes move towards pathogens and recognise the antigens on the surface of the pathogen as being non-self

cell surface membrane of a phagocyte extends out and around the pathogen, engulfing it and trapping the pathogen within a phagocytic vacuole known as endocytosis

Enzymes are released into the phagocytic vacuole when lysosomes fuse with phagosome
These digestive enzymes, which includes lysozyme, digest the pathogen
After digesting the pathogen, the phagocyte will present the antigens of the pathogen on its cell surface membrane

presentation of antigens initiates the specific immune response

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19
Q

what are phagocytes also known as

A

antigen presenting cell

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20
Q

what do antigens do

A

allow cell-to-cell recognition

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21
Q

what happens to the antigens of the engulfed pathogen

A

phagocytes transfer the antigens of the digested pathogen to their cell surface membrane, becoming antigen presenting cells

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22
Q

what do antigen presenting cells do and how

apc=sir

A

Antigen presenting cells such as macrophages activate the specific immune response

This occurs when the white blood cells of the specific immune response, known as lymphocytes, bind to the presented antigens with specific receptors on their cell surface membranes

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23
Q

what are the Y shaped antibodies also known as

A

immunoglobulins

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24
Q

how many polypeptides do antibodies consist of

A

four polypeptide chains; two ‘heavy’ chains attached by disulfide bonds to two ‘light’ chains

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25
Q

what does each polypeptide consist of

A

a constant region and variable region
The amino acid sequences in the variable region are different for each antibody

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26
Q

what is there at the end of each variable region

A

a site called the antigen binding site
The antigen binding sites vary greatly, giving the antibody its specificity for binding to antigens

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27
Q

what does variable region do

A

where the antibody binds to an antigen to form an antigen-antibody complex

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28
Q

what is the hinge region

A

where the disulfide bonds join the heavy chains, gives flexibility to the antibody molecule provides flexibility to the molecule and allows the molecule to change shape which is helpful in binding to antigens of different shapes and sizes.

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29
Q

what do membrane bound antibodies have

A

an extra section of polypeptide chain within their heavy chains which forms the attachment to lymphocytes

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30
Q

what can the gene that codes for heavy chain antibodies in non membrane bound antibodies do

A

undergo a process called alternative splicing to remove this extra section in non-bound antibodies removes coding sections called exons

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31
Q

what are the three ways antibodies deal with pathogens

A

antibodies can bind to the receptors of host cell, preventing pathogens from infecting host cells

act as anti-toxins by binding to toxins produced by pathogens

cause pathogens to clump together, a process known as agglutination; this reduces the chance that the pathogens will spread through the body and makes it possible for phagocytes to engulf a number of pathogens at one time

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32
Q

What are T cells and where are they produced

A

a type of white blood cell

produced in the bone marrow and finish maturing in the thymus, which is where the T in their name comes from

33
Q

what do mature T cells have

A

specific cell surface receptors called T cell receptors
have a similar structure to antibodies and are each specific to a particular type of antigen

34
Q

when are t cells activated

A

Bacterium is engulfed by a macrophage. Antigens are displayed on the surface of the macrophage

The macrophage acts as an antigen-presenting cell (APC).

Macrophage APC binds to T Helper cell with complementary receptor proteins.

The T Helper cell is ‘activated’ and divides by mitosis to form T memory cells and active T helper cells.

35
Q

what could antigen presenting cell be

A

a macrophage, an infected body cell, or the pathogen itself

36
Q

how do t cells increase in number

A

Dividing by mitosis produces genetically identical cells, or clones, so all of the daughter cells will have the same type of T cell receptor on their surface

37
Q

what happens as t cells divide by mitosis

A

differentiate into three main types of T cell

T helper cells

T killer cells

T memory cells

38
Q

what is a T helper cells

A

Release chemical signalling molecules that help to activate B cells

39
Q

what is a T killer cells

A

Bind to and destroy infected cells displaying the relevant specific antigen

40
Q

what is a T memory cells

A

Remain in the blood and enable a faster specific immune response if the same pathogen is encountered again in the future

41
Q

where are b cells found

A

B cells remain in the bone marrow as they mature, hence the B in their name

42
Q

what do b cells have

A

specific receptors on their cell surface membrane
The receptors are in fact antibodies, and are known as antibody receptors
Each B cell has a different type of antibody receptor, meaning that each B cell can bind to a different type of antigen

43
Q

what happens when b cell binds to antigen and

A

forms an antigen-antibody complex

44
Q

what does daughter cells of B cell differentiate to

A

Effector cells, which go on to form plasma cells
Plasma cells produce specific antibodies to combat non-self antigens

Memory cells
Remain in the blood to allow a faster immune response to the same pathogen in the future

45
Q

what do eukaryotic cells transcribe

A

both introns and exons to produce pre-mRNA molecules

46
Q

what happens before pre-MRNA exit nucleus

A

splicing occurs
The non-coding intron sections are removed
The coding exon sections are joined together
The resulting mRNA molecule contains only the coding sequences of the gene
Since these modifications are made after transcription occurred, they are called post-transcriptional modifications

47
Q

what is alternative splicing

A

exons of genes can be spliced in many different ways to produce different mature mRNA molecules

a single eukaryotic gene can code for more than one polypeptide chain

48
Q

what happens when a new antigen is encountered

A

primary immune response consisting of a non specific response then specific response

49
Q

if it is the first time the immune system has encountered an antigen what would you expect for the number if T and B cells

A

T and B cell number with correct membrane receptor present in blood will be low

50
Q

why does person get symptoms for disease first time they contract it

A

takes time for correct T and B cells to be activated and to divide and differentiate into different cell types

plasma can take days to develop and produce antibodies

51
Q

what allows someone to be immune to a pathogen

A

memory cells during primary response

52
Q

HIV evasion mechanism

A

Virus kills helper T cells after it infects them which reduces number of cells that could detect the presence of a virus and produce antibodies

High antigenic variability due to high mutation rate in genes coding for antigen proteins - memory cells for one strain wont recognise antigen for another strain

Virus prevents infected cell from presenting antigens on cell surface membrane making it difficult for WBC to recognise and destroy the infected cells

Disrupts antigen presentation in infected phagocytes making it difficult for immune system to recognise and destroy the cells

53
Q

TB evasion mechanism

A

once engulfed by phagocyte in lungs the bacteria produces substances which prevent lysosomes from fusing with phagocytic vacuole preventing bacteria from being broken down by digestive enzymes making them multiply

54
Q

How do antibiotics work

A

interfering with growth or metabolism of target bacterium

55
Q

why will mammalian cells not be damaged by antibiotics

A

eukaryotic with no cell walls, different enzymes and different ribosomes

56
Q

why wont viruses be affected by antibiotics

A

no enzymes ribosomes or cell walls

57
Q

explain effect of increasing interferon dosage on survival from influenza virus

A

increasing dose of interferon increases the survival time of the mice
because interferon inhibits viral replication (inside cells)
the greater the dose of interferon the fewer virus particles {produced / released} (to infect other cells)

58
Q

what is bactericidal antibiotics

A

kill bacteria by destroying their cell wall causing lysis (burst)

59
Q

what is bacteriostatic antibiotics

A

inhibit growth of bacteria by stopping protein synthesis and production of nucleic acid so bacteria cant divide and grow

60
Q

devise an experiment to investigate the effects of different antibiotics

A

Set up your sterile work area by wiping surfaces with disinfectant and setting up a Bunsen burner

Transfer some of the bacterial culture on to an agar plate using a sterile pipette and spread it out using a inoculating loop

Soak similar sized paper discs in different types of antibiotics

Add a negative control to the investigation by soaking a disc in distilled water

Space the discs apart on the agar plate using sterile forceps

Lightly tape a lid onto the petri dish, invert and incubate at 25 °C for 24 to 48 hours

Any clear patches in the lawn will indicate where bacteria could not grow - This is called the clear zone

61
Q

why lightly tape than sealing lid
why invert the dish
why incubating at room temperature

A

ensures oxygen is available to bacteria

prevents condensation from dripping onto the agar, potentially contaminating the dish

prevents the growth of harmful pathogens

62
Q

what is the use of the bunsen burner in experiment

A

updraft and prevent microorganisms in air from landing in the work area

63
Q

what does a larger clear zone indicate

A

more effective antibiotic was at inhibiting bacterial growth

64
Q

characteristics of antibodies

A

reference to glycoprotein;

credit detail of structure e.g. specific (3D) shape, L and H regions, Y-shape, 4 (peptide) chains, disulphide bridges between peptides, hinge region

reference to {antigen-binding site / variable region / Fab (region) / eq };
idea of antibodies have a {similar / constant / Fc / eq } region;

produced by plasma cells / present on B cells;

role of antibody described e.g. opsonisation, immobilisation, agglutination, lysis ;

65
Q

what is active immunity

A

when an antigen enters the body triggering a specific immune response

66
Q

what is active natural

A

acquired through exposure to pathogens

67
Q

what is active artifical

A

acquired through vaccination

68
Q

what is passive immunity

A

acquired without an immune response; antibodies are gained from another source, not produced by the infected person

69
Q

what is passive natural

A

Foetuses receive antibodies across the placenta from their mothers
Babies receive antibodies in breast milk

70
Q

what is passive artificial

A

People can be given an injection / transfusion of antibodies

71
Q

what is antigenic variation

A

memory cells do not detect the altered antigens and are no longer effective against the pathogen

72
Q

explain how phagocytosis and lysosome action lead to antigen presentation by macrophages

A

pathogen taken into macrophage
phagosome fuses with lysosome
lysosome digests the bacteria
antigen / bacteria is presented on the surface of the macrophage

73
Q

difference between totipotent and pluripotent

A

totipotent cells can { give rise to / differentiate to become } { any cell / extra embryonic tissues / eq };

pluripotent cannot { give rise to / differentiate to become } { all cells in the body / extra embryonic tissues / eg };

idea that only totipotent cells can give rise to other totipotent cells;

idea that totipotent cells can give rise to an entire human being, pluripotent cells cannot;

74
Q

Give two differences between the genetic material of bacteria and viruses.

A

bacteria have DNA, viruses have DNA or
RNA ;
2. idea that bacteria have {circular / eq}
genetic material, viruses have {linear /
straight} ;
3. bacterial DNA is double-stranded, viral {DNA
/ RNA} is single (or double) stranded / eq;
4. bacteria (may) have plasmids, viruses do
not have plasmids

75
Q

Describe how a B cell is activated.

A

{antigen / bacteria / virus / pathogen} {binds / eq} to B
cell ;
2. {antigen / bacteria / virus / pathogen} {binds / eq} to
MHC (antigen) ;
3. T helper {lymphocytes / cells} {bind / eq} (to B cell) ;
4. reference to cytokines (from T helper cells)

76
Q

how do macrophages present antigen to helper T cells

A

macrophage {binding/ eq} to T (helper) {cell /
lymphocyte} ;

  1. reference to {MHC / major histocompatibility complex }
    (on macrophage) ;
    as antigen is presented on MHC
77
Q

How does HIV enter T helper cells

A

(glycoproteins / GP120} on the (surface of the) virus(1)

bind to (CD4) receptors on the (surface of the) T (helper) cells(1)

viral envelope fuses with cell membrane of T helper cell (1)

viral RNA enters the cell

78
Q

Explain why the presence of microorganisms on the skin and in the gut helps to prevent pathogenic organisms multiplying in the body.

A

flora in the gut and skin are better adapted to the conditions (1)
* therefore they can outcompete pathogenic organisms (1)
* bacteria in the gut secrete {chemicals /lactic acid} which help to destroy pathogens (1)

79
Q

Devise a laboratory procedure to compare the effectiveness of penicillin with one of the new antibiotics.

A

prepare agar plates with bacterial cultures / bacterial lawn / seeded with bacteria -use bacteria that are resistant to other antibiotics

prepare solutions of new antibiotic and penicillin
place onto paper discs / into wells in the agar /

prepare mast rings control time and temperature of incubation

same concentration and volume of both antibiotics
measure the area of inhibition

repeat for effective antibiotics

description of serial dilution of each antibiotic range of dilutions on each plate-one antibiotic per plate

statistical test to determine which is the most effective

repeat with different strains of resistant bacteria

Biology Mock AS 2 (23 decks)

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