6B Microorganisms and Immunity Flashcards
(83 cards)
1
Q
immune system
A
biological processes that identify and kill pathogens
2
Q
phagocytosis
A
engulfment and digestion of pathogens by w.b.c
3
Q
bone marrow
A
site of B cell maturation
4
Q
mast cells
A
immune system cells -> release histamine
5
Q
T helper cells
A
release substances to activate …
- B cells
- T killer cells
- macrophages
6
Q
Tuberculosis
A
- infectious disease of respiratory system
- caused by Mycobacterium TB
7
Q
HIV
A
virus causing AIDS -> infects and destroys T helper cells (host cell)
8
Q
AIDS
A
- disease of human immune system
- increases chance of other diseases (infections, cancer)
9
Q
immunity
A
having sufficient B and T memory cells to avoid disease
10
Q
booster injections
A
re-exposure to antigen
- increases no. B and T memory cells to maintain protective levels so more antibodies
11
Q
herd immunity
A
when high enough proportion of pop is vaccinated that those without immunity are PROTECTED
12
Q
bacteriCIDAL
A
antibiotics that destroy bacteria
13
Q
bacterioSTATIC
A
antibiotics that prevent MULTIPLICATION OF BACTERIA
14
Q
antigenic drift
A
changes in antigens due to mutations in pathogen
15
Q
what is the name of the markers on microorganisms that allow cell-to-cell recognition?
A
antigens
16
Q
self antigens
A
produced by own body
DON’T STIMULATE IMMUNE RESPONSE
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
18
Q
what do antigen presenting cells
(eg. macrophages) do?
A
activate specific immune response
-> occurs when lymphocytes bind to presented antigens
19
Q
macrophage
A
type of phagocytic w.b.c
long lived
20
Q
bacteria
A
- single-celled
- prokaryotic
21
Q
pathogen
A
organism that causes disease
diseases caused by pathogens = infectious
22
Q
describe how HIV affects immune system
what does it mean 2 RNA strands????
A
HIV replicates inside host T helper cell
- attachment protein attaches to CD4 receptor on cell membrane of T helper cell
- capsid released into cell -> uncoats and releases RNA into cell’s cytoplasm
- inside cell: REVERSE TRANSCRIPTASE used to make COMPLEMENTARY STRAND of DNA from viral RNA template
- from this, DOUBLE STRANDED DNA made and INSERTED into human DNA
- viral proteins assembled into new viruses -> bud from cell and go to infect other cells
23
Q
inflammation
A
site where pathogen enters body
24
Q
describe inflammation process
A
- immune system cells recognise foreign antigens on surface of pathogen and release HISTAMINE THAT TRIGGERS INFLAMMATION
- histamine causes VASODILATION (widening of ARTERIOLES) around site -> increases blood flow to it
- molecules also increase PERMEABILITY OF CAPILLARIES
- -> increased blood flow = brings loads of immune system cells to site-> increased permeability = allows cells to move OUT OF BLOOD->INFECTED TISSUE
- immune system cells start to destroy pathogen
25
what are the body's barriers to prevent infection?
- 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)
26
what are initial symptoms of AIDS?
- minor infections of mucous membranes (inside of nose, ears, genitals)
- recurring respiratory infections -> caused by lower than normal no. of T helper cells
27
symptoms of AIDS later on?
- as AIDS progresses = less and less T helper cells
- patients become prone to more serious infections eg. chronic diarrhoea and TB
28
passive immunity
acquired without an immune response
antibodies gained are from another source e NOT OWN BODY
29
artificial passive immunity
injection / transfusion of antibodies e.g. the tetanus antitoxin
30
artificial active immunity
vaccination
31
natural active immunity
exposure to a pathogen
32
natural passive immunity
antibodies received from another organism eg. from placenta or breastmilk
33
role of T helper cells in developing immunity after a vaccine
- T helper cells BIND to APC
- leads to production of ACTIVE T- helper cells
- T helper cells activate B cells to become PLASMA CELLS
34
specific immune response
| secondary response
DELAYED response directed at SPECIFIC pathogen
35
non-specific immune response
| primary response
IMMEDIATE response directed at ALL pathogens
36
suggest how antihistamines work
bind to histamine receptors and BLOCK histamine from binding
37
explain why someones wound may become hot, red and swollen
hot -> increase in metabolic rate and lots of cells RESPIRING
red -> increased blood flow
swollen -> leakage of fluid from CAPILLARIES
38
interferons
- anti viral proteins
- made by cells when infected with virus
- **prevent virus spreading** to uninfected cells
39
how do interferons prevent virus from spreading to uninfected cells?
- **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
2 main types of lymphocytes
- B cells
- T cells
41
neutrophils
type of phagocyte
short lived
42
lysosomes
membrane organelles
contain digestive enzymes called lysozymes -> digest unwanted material present in cells
43
pus is a sign of what?
dead neutrophils
44
B cells divide to produce two clones of cells ...
- B effector cells
- B memory cells
45
B effector cells
**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
B memory cells
remain in body for years
enable organism to respond quicker to same antigen in future
47
cell clonal selection
process of B cell division
48
**antibodies**
- secreted by plasma cells
- bind to specific antigens identifying them for easier destruction
- and **agglutinating** them so phagocytosis is quicker
49
granuloma
anaerobic masses of tissue containing dead bacteria and macrophages
50
T cells
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
T killer cells
bind to antigens and destroy their infected cells
52
T memory cells
remain in blood
-> enable faster specific immune response if same pathogen encountered again in future
53
what role to **cytokines** play in making sure there are enough
**T killer cells**?
## Footnote
is this answer right???
stimulate differentiation of T cells
54
**(compare and contrast B and T cells)**
## Footnote
check if this is right
- 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
compare and contrast bacteria and viruses
- 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
what are the 4 entry points for pathogens?
- broken skin -> access to tissues and bloodstream
- dig system -> contaminated food / drink
- respiratory system -> inhaling
- mucosal systems eg. inside of nose, mouth, genitals
57
histamine
chemical signalling molecule that enables **cell signalling** / communication between cells
stimulates:
- vasodilation
- leaky capillary walls
- phagocytosis
58
what does the **non**-specific immune response include?
## Footnote
happens first!!
- **inflammation**
- **interferon production** -> prevents virus spreading to uninfected cells
- **phagocytosis** -> WBCs engulf pathogens
- **lysozyme action** -> kills bacteria cells by damaging cell wall
59
describe the process of phagocytosis
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
what does the specific immune response include?
- phagocytes activate T cells
- T helper cells activate B cells
61
what are cytokines?
**chemicals** that **T helper cells release**
to stimulate **÷** and **differentiation** of **B cells**
62
describe the process of activation of T helper cells
## Footnote
is this exactly what i need to know?
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
compare and contrast the humoral response and the cell mediated response
## Footnote
check if right
- 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
explain why a person newly infected with TB may not show any symptoms
immune system 'seals off' **infected phagocyte** in structures (in lungs) called **tubercles**
-> bacteria become **dormant** in there so person shows no symptoms
65
describe how *Mycobacterium tuberculosis* causes TB
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
explain the role of APCs
## Footnote
just ask about this whole card -> is it right??
- 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
## Footnote
check
67
name the 2 types of specific immune response
- humoral
- cell mediated
68
how do antibodies help to clear an infection?
- **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
differences between structure of **membrane-bound** and **secreted** antibodies
membrane bound have **extra section of protein** on **heavy chain** that **anchors them** to B cell membrane
70
membrane bound antibody
attached to membrane of **B cell**
71
secreted antibody
free from attachment
72
why is non-specific / primary response **slow**?
aren't many B cells that make antibody needed to bind to antigen
73
HIV evasion mechanisms
- 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
why are infections caused by antibiotic-resistant bacteria more common in hospitals?
- more antibiotics used there
- so **bacteria** in hospitals **more likely** to have **evolved** resistance against them
75
how do hospitals prevent and control HAIs caused by antibiotic-resistant bacteria?
- 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
describe what ribsosomes do in bacterial cells
produce proteins **from mRNA**
77
devise an experiment to determine the effect of diff antibiotics on bacteria
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
Mycobacterium tuberculosis evasion mechanisms
- **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
introns
sections of **gene** that **don't code for a.a**
80
exons
sections of gene that **do code for a.a**
81
explain how **one gene** can give rise to **more than one protein** through **post-transcriptional changes to mRNA**
(4 marks)
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
describe some codes of practice hospitals use to prevent and control HAIs
- 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
HIV requires a host cell to replicate.
suggest why it needs a host cell
**doesn't have** stuff eg. **enzymes + ribosomes** to replicate on its **own**
