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POM > Immunology and Infection > Flashcards

Immunology and Infection Flashcards

1
Q

what are viruses

A

Not cells by themselves
Obligate parasites
RNA or DNA
replicate using host-cell nuclear machinery,
host specificity
divide by budding out of the host cell if an enveloped virus, cytolysis if a non-enveloped virus
faecal-oral, airborne, insect vectors, blood borne

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2
Q

example of a virus

A

HIV virus
HIV virus binds to host cell receptor causes fusion to empty its virion inside. The genetic material in HIV is RNA which is transcribed to DNA via reverse transcription. DNA is the integrated into the host genome, activation leads to transcription of the DNA and translation to make the protein virus and contents which assemble and bud out of the cell

other examples: smallpox, polio

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3
Q

what are bacteria prokaryotes vs eukaryotes

A

prokaryotes dont have internal membranes, eukaryotes have internal membranes to compartmentalise and define organelles
prokaryotes are haploid, eukaryotes can be hap or dip
prokaryotes have a poorly defined cytoskeleton, eukaryotes well defines
prokaryotes cell wall contains peptidoglycan
prokaryotes divide by binary fission, eukaryotes by mitosis and meiosis
prokaryotes have circular chromosome of DNA, no nucleus

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4
Q

name some structures found in bacteral prokaryotes

A

pilus- to adhere to surfaces

flagellum- moved towards chemical gradient

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5
Q

Example of a prokaryote

A

Shigella species: no flagella, faecal-oral transmission and causes bloody diarrhoea. invades gut and destroys, spreads cell to cell using the hosts actin. shigellos

neisseria meningitidis- community acquired gets into blood stream: can cause colonisation, septicaemia or meningitis. rapid progression, septic shock and severe inflam response

clostridium difficile, methicillin resistant staph aureus

tuberculosis: air-borne but new drugs to combat resistance, better vaccines and tools for early diagnosis

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6
Q

What is more significant, mutation rates or generation time

A

Although point mutation rates is only slightly more frequent in viruses (which means the mutations don’t get corrected and there are lots of variations), the generation time is very short for bacteria

similar mutation rates but short generation time

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7
Q

what are fungi

A

eukaryotic
cutaneous, mucosal or systemic infection cause infections known as mycoses
yeast, filaments or both
yeasts bud or divide, filaments/hyphae have cross walls or septa

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8
Q

example of a fungi

A

candida albicans causes thrush and vaginal yeast infections

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9
Q

What is a protazoa

A

unicellular eukaryotic organisms
intestinal, blood and tissue parasites
replicate in host by binary fission or formation of trophozoites (infect others then replicate there) inside a cell
ingestion or through vector

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10
Q

examples of protazoa

A

plasmodium species aka malaria: via mosquito vector, blood and tissue parasites, form trophozoites

leishmania species- leishmaniasis: sandfly infects, causes blood and tissue parasites, form trophozoites

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11
Q

what are helminths

A

metazoa with eukaryotic cells: multi cellular theyre visible to human eye, have life cycles outside of the human host

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12
Q

examples of helminths

A

round, flat and tapeworms
flukes: schistosomiasis where snails are infected with miracidium, become an adult, spike humans in lakes and lay eggs in HPV

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13
Q

What are primary lymphoid tissues and whay are made

A

where lymphopoeisis occurs : makes B, T NK cells

bone marrow, thymus and foetal liver

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14
Q

What immune response are B and T cells a part of

A

adaptive

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15
Q

what are the two hallmarks of lymphocytes

A

1) SPECIFICITY : unique b and t receptors

2) MEMORY: rapid expansion

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16
Q

How are B cells made during infection

A

during infection, white cell production increases as the bone marrow is already full of haematopoeitic precursor cells

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17
Q

what is the difference in which bones produce white cells in the foetus and adult

A

Foetus is all bones in the marrow, very cellular. occurs in liver and spleen too.

in adults, mostly have flatbones so occurs at the end of flatbones, in vertebrae, iliac bones and ribs. in bone marrow (red bone marrow) and fat (yellow bone marrow)

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18
Q

where does the final maturation of the b cell occur

A

periphery

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19
Q

what is b cell repertoire and where is it made

A

repertoire is the range of distinct b or t cells in a host

b cell repertoire is formed in bone marrow

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20
Q

How are T cells made: what types of selection are there

A

Made in bone marrow, but immigrate to the thymus
POSITIVE SELECTION: if T cell can signal and recognise MHC
NEGATIVE SELECTION: if reacts against own body

if the T cell fails it undergoes apoptosis, if gets through positive and negative selection then exits thymus

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21
Q

what can affect the output of the thymus

A

age: thymic involution wheere the thymus shrinks with age: change in structure and reduced mass

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22
Q

What are secondary lymphoid organs: describe and name

A

where lymphocytes can interact with antigens and other lymphocytes, are distributed widely across body so cells are close to antigens, interconnected via lymph system and blood
spleen, draining lymph nodes, GI mucosa, appendix, peyers patches, adenoids

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23
Q

what is the difference between lymph nodes/adenoids and the spleen

A

Lymph nodes and adenoids are DISCRETE ORGANS (encapsulates tissue)
Spleen is a DISTINCT REGION WITHIN A TISSUE

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24
Q

describe how lymph nodes filter antigens and from where

A

afferent LYMPH flows into lymph nodes, theres a medullary sinus which lymph can flow into and pass t and b zones
the T cell layer is the inner layer and the B cell layer is the outer layer called lymphoid follicles which also contain germinal centres

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25
Q

describe how the spleen filters pathogens and from where

A

spleen has an arterial connection, filters BLOOD The spleens red pulp is where red blood cells are made, the inner white pulp is where arterial blood flows
the T zone located centrally (also called the periarteriolar lymphoid sheath or PALS) and the B cells distributed around the T zone in tightly packed follicles that have germinal centres inside.

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26
Q

What is the epithelial barrier

A

first line of defence against infection, is a physical barrier, has an extensive lymphatic network to drain antigen away.
includes GI and respiratory lining not just skin

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27
Q

Within the gut there are specialised secondary lymphoid tissues called what

A

peyers patches, below epithelium of small intestine. Are follicles enriched with B cells, lots of germinal centres

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28
Q

what are germinal centres

A

where B cells undergo mutation and selection to make high affinity antibodies

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29
Q

The tonsils make what ring

A

waldeyer ring which have lots of germinal centres

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30
Q

how do lymphocytes circulate, if the T cell is far from an antigen what happens

A

through blood and lymph, Naive t cells recirculate once every 24 hours. constant flow, if the T cell specific for an antigen is far from antigen the naive t cells will differentiate or secrete signals

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31
Q

what is extravasation of naive t cells

A

where effector T cells migrate through the endothelial cell wall of blood vessels called High endothelial venules into inflamed tissues
on the blood side, Selectins bind causing rolling, the cell is activated and integrins bind LFA-1 and Mac-1 which binds to ICAM which allows transmigration into the lymph node.
chemokines release ccr7 and ccl21 to provide chemotactic signals

1) chemo attraction : cytokines up regulate adhesion molecules called selections
2) rolling adhesion: Carbohydrate ligands in a low affinity state on neutrophils bind to P and E selecting. Activates the cell
3) tight adhesion: chemokine promote low to high affinity switch in the integrins LFA-1 and Mac-1 which enhance the binding to ligands like ICAM-1
4) Transmigration: Cytoskeletal rearrangement and extension of membrane mediated by PECAM

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32
Q

what would happen if there was a wound in the skin

A

dendritic cells present within the skin, they present antigens on MHCI or MHCII
langerhans in epidermis and dendritic cells in dermis. dendritic cells migrate via afferent lymph into lymph nodes

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33
Q

What is prontosil

A

bacteriostatic- Gram +
sulphonamide antibiotic
UTIS- targets folic acid synthesis

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34
Q

What is linezolid

A

targets positive bacterias 50S rRNA subunit to stop protein synthesis
bacteriostatic

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35
Q

what is daptomycin

A

bactericidal

targets gram + cell membrane

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36
Q

what are macrolides

A

+ and -
50S subunit targeted stops amino acyl tranfer
bacteriostatic

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37
Q

what is an antibiotic

A

antimicrobial agent produced by a microorganism to kill or inhibit other microorganisms

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38
Q

what is antimicrobial, antiseptic, bacteriocidal and bacteriostatic

A

antimicrobial: selectively kills or inhibits microbes
antiseptic: selectively kills or inhibits microbes but used topically to prevent infection
bacteriocidal: kills bacteria
bacteriostatic: stops bacteria growing

39
Q

what does antibiotic resistance cause

A 
increased time for effective therapy 
additional approached needed
expensive therapy aka IV
more toxic drugs 
less effective antibiotics
40
Q

what are aminoglycosides

A

gentamicin, streptomycin
bactericidal
target protein synthesis, affect 30S subunit to alter RNA proofreading and cause damage to cell membrane

41
Q

what is rifampicin

A

bacteriacidal
RpoB subunit or RNA polymerase to stop transcription
red/orange faeces

42
Q

what is vancomycin

A

bacteriacidal

targets lipid II component of cell wall, crosslinks via d-alanine residues

43
Q

how do beta lactams work

A

interfere with synthesis of petidoglycan component of cell wall which kills them.
bind to penicillin binding proteins

44
Q

what is selective toxicity

A

difference between bacteria and mammals allows for many processed that AB’s can target
e.g cell wall synthesis (penicillin, vanomycin), inhibit protein synthesis (macrolides like erythromycin/ aminoglycosides like streptomycin), inhibition of nucleic acid replication (quinolones-rifampin), plasma membrane, synthesis of metabolites (sulfanilmide and trimethoprim)

45
Q

what are quinolones

A

synthetic broad spectrum
bacteriacidal
DNA gyrase in gram -, topoisomerase in gram +

46
Q

what is resistance

A

if resistant strains can grow above the clinical breakpoint (minimal inhibitory concentration is the lowest concentration of AB’s required to inhibit growth)

47
Q

how is antibiotic resistance driven

A

population naturally has Ab resistant genes due to mutations and acquired DNA, there is slow growth. Without any selection pressure the AB resistance has no advantage and their mutation may come at a fitness cost so they wont need to replicate more so low prevalence.
however, if there is selection pressure e.g antibiotics given then the resistant mutations outcompete and will survive leading to a high prevalence of resistant strains

48
Q

through what four mechanisms does antibiotic resistance occur

A

1) altered target site
2) inactivation of antibiotic
3) altered metabolism
4) decreased drug accumulation

49
Q

examples of altered target sites

A

acquire a gene that encodes a target modifying enzyme e.g. methicillin res staph aureus endocdes PBP2a (llow affinity for beta lactams) instead of PBP

e.g.2. steptococcus pneumoniae acquires the erm gene so AB target site is methylated

50
Q

examples of antibiotic being inactivated

A

enzymatic degradation or alteration
beta-lactamase
ESBL and NDM-1 are broad spectrum beta lactamases

51
Q

what is altered metabolism and examples

A

increased production of enzyme substrate so it out competes for AB inhibitor
inc PABA stops sulfonamides
or bacteria switch to other metabolic pathways

52
Q

what is decreased drug accumulation

A

reduced penetration of Ab into bacterial cell OR increased efflux of AB out so drug cant reach concentration

53
Q

source of AB resistant genes

A

plasmids- have resistance to many AB’s so if plasmid survives then resistance to multiple phenotypes
transposons- intergrate into chromosomal DNA, transfer of genes from plasma to chromosomes
Naked DNA- from dead bacteria into environment

54
Q

how do AB resistant genes spread from their sources

A

1) TRANSFORMATION: uptake extracellular DNA
2) CONJUGATION: share plasmid between two bacteria
3) TRANSDUCTION: phages share the DNA

55
Q

why mechanisms of resistance treatment may be hard

A

if they have a biofilm or a shielded intracellular location
if grow slowly then might not be many processes to inhibit
spores are resistant to heat, antibiotics and antiseptics
persister cells become dormant

56
Q

reasons for tratment failure

A 
wrong gram + or - choice 
AB cant penetrate target site 
Inappropriate dose due to half lifes 
Inappropriate administration 
AB resistance
57
Q

risk factors of hospital acquired infection

A 
high numbers of ill people 
crowded wards 
broken skin 
indwelling devices like catheters
AB might suppress normal flora so pathogen has no competition leads to overgrowth anf damages host
staff
58
Q

how to reduce resistance

A 
less AB prescribed 
less broad spectrum AB's 
quicker identification of resistant strain infection 
combination therapy 
know local strains

surveillance: usage and resistance surveillance
research: basic science, epidemiology, social drivers
interventionn: regulation, infection prevention, education

59
Q

How does a gram stain work and what would a purple stain mean vs a pink stain

A

Purple stain is gram positive
gram positive has one outer membrane and THICK peptidoglycan
in the gram positive the wall is thick so the crystal violet and iodine complex cant be washed out

pink stain is gram negative
gram negative have two outer membranes and THIN peptidoglycan
the crytal violet and iodine complex can be washed out so when safranin is applies becomes pink

60
Q

Culture test - haemolysis only works on what bacteria and what does it show

A

gram positive
Gamma-hemolysis if no impact on red blood cells
Alpha-haemolysis if theres a green zone as it means some haemolysin has been released
Beta- haemolysis if transparent zone arround

61
Q

what is a lactose test and what type of bacteria is it used on

A

gram negative
If bacteria is lactose fermenting produces lactic acid making the colonies pink, if its a non fermenter will be colourless

62
Q

catalase test is used on what types of bacteria and what does it do

A

positive
catalase positive bacteria will produce bubbles and means its staphlococci
catalase negative will produce no bubbles and be streptococci

63
Q

coagulase test is used on what and what does it show

A

gram positive, checks if can form coagulase

if clumps form its positive and is staph aureus

64
Q

What is the difference in how b and T cells recognise antigens

A

T cells recognise linear epitopes in the context of MHC, an epitope being the region where.a receptor binds.
B cells recognise 3D structure, antibodies recognise structural epitopes

65
Q

how does clonal expansion occur

A

each lymphocyte has a unique receptor. interacts with foreign molecule, the t cell that matches is activated leading to clonal expansion where each differentiated effector cell will have the same receptor

66
Q

how is antigen diversity generated

A

recombination

immunoglobulin gene rearrangement: each BCR chain is encoded by separate multigene families on different chromosomes

67
Q

describe the t cell receptor

A

an alpha and beta subunit on the Fab region. bottom of alpha and beta chains is called the constant region, the tips are called the variable region which is made by gene reassortment
recognises antigen fragments presented on MHC molecules

68
Q

what is the role of MHC

A

defining self and not cell, presents antigens

is critical in donor matching

69
Q

difference between MHCI and MHCII

A

MHCI is all nucleated cells. encoded by one gene. has a single alpha chain a1 a2 in variable region then a3 in constant. next to a3 is a common beta microglobulin which is the same in all MHCI.: MHCI is a screening mechanism for what’s inside cell
MHCII is only on professional antigen presenting cells like dendritic or macrophage, encoded by 2 genes has an alpha and beta chain

70
Q

what is MHC encoded by, and describe

A 
HLA genes. 3 class I and class II loci 
co dominant maternal and paternal
71
Q

what type of T cells react with MHCI and MHCII, what do they look for

A

CD8 bind to MHCI : CD8 on surface of T cells makes MHCI show peptides to T cell receptor looks for intracellular infection
CD4 bind to MHCII: CD4 on surface of T cells makes MHCII show its peptides and looks at the peptides that have been taken in from extracellular spaces

72
Q

How do CD4 cells fight infection

A

recruit cytokines which influence immune response.
e.g Th17 is pro inflam for bacterial and fungal
Th1 is pro inflam, boosts cellular response- IL12
Th2 is proallergic - IL4, 5,13
Treg is anti inglam IL-10

HIV blocks CD4 cells

73
Q

How do CD8 cell fight infection

A

kill cells via apoptosis. CD8 cells store perforin, granzymes and ganulysin in cytotoxic granules. after they recognise theres non self protein they release these: perforin forms pores and the granzymes enter the cell to fragment to dna

74
Q

what is the antibody structure

A

has two long heavy chains (middle two) and two light chains that look like theyre added to the top of these.
the constant region is just the lower heavy chain part DRIVES THE FUNCTION
the variable region is the very tips of both chains and is what BINDS TO THE PATHOGEN

75
Q

What are the three ways antibodies can work

A

NEUTRALISATION: Fab mediated as they bind to the pathogen to stop it getting into cells
OPSONISATION: Fc mediated as makes the antibody-pathogen complex more attractive to macrophages
COMPLEMENT ACTIVATION: antibody activates complement to enhance opsonisation

76
Q

differences between IgG, IgM, IgA, IgD, IgE

A

IgG is the main antibody in blood, highest opsonisation and neutralisation activity, IgM is made upon first antigen invasion, IgA in mucosal linings
IgD we dont know, IgE in allergy

77
Q

what does the unique binding site of the B bind to

A

antigenic determinant aka EPITOPE

78
Q

Naive antigen specific lymphocytes need what to activate them, how do the different activation pathways change the antibody

A

cant just be activated by soluble antigen
Naive B cells need an accessory signal from a helper T cell (thymus dependent) make IgG classes and have memory
OR directly from microbial constituents to make IgM antibodies (Thymus independent) no memory.

79
Q

How is thymus independent and thymus independent activation different

A

Thymus dependent activation occurs when B cell receptor recognises antigen, internalised it and breaks it down into peptides, the peptides associate with self molecules MHCII and is expressed at the cell surface which CD4 T helper cells recognise
Thymus independent activation occurs due to antigens which are polysaccharide and have repetitive structures, require second signal PAMP like LPS

80
Q

what is immune regulation and why is it needed

A

control of immune response to stop inappropriate reactions

needed to avoid excessive lymphocyte activation and tissue damage, prevent inappropriate reactions against self antigen

81
Q

what are the causes of a failing immune regulation

A

autoimmune disorders
allergy
hypercytokinemia and cepsis

82
Q

What is autoimmunity

A

immune response against self antigen.

83
Q

examples and features of autoimmune diseases

A

chronic diseases with prominent inflammation
can be systemic like lupus or organ specific like graves

features: imbalance between immune activation and control: susceptibility genes and environmental influences

84
Q

autoimmunity can be caused by

A

immune responses against self = autoimmunity, against microbial antigens = crohns
immune response inappropriately directed or controlled
t cells and antibodies mayc ause
self perpetuating

85
Q

allergy is another failure of immune regulation what happens

A

harmful response to non infectious antigens cause tissue damage and disease

IgE and mast cells mediate cause acute anaphylactic shock
T cells can cause delayed type hypersensitivity 4

86
Q

what happens in hypercytokinemia and sepsis

A

too much immune response, positive feedback loop, pathogens enter wrong compartment

87
Q

describe the phases of cell mediated immunity

A

INDUCTION: dendritic cell ingests infected material, presents on MHCII, dendritic cell moves into lymph node and presents its antigen-MHCII complex to t cells. T cell will be activated and clonally expand
EFFECTOR PHASE: T cells return and migrate to site of infection, kills and removes antigen
MEMORY: effector pool contracts to form memory pool which shuts down immune response

88
Q

What is self-limitation

A

the decline of immune responses, happens when the antigen that initiated the response is eliminated. memory cells are the only survivors

89
Q

what is needed to cause a response to infection

A

antigens must be recognised
co-stimulation of b cell
cytokine release

cell then responds

90
Q

when are active control mechanisms used

A

if persistent antigen like self antigens, active control mechanisms are used to limit the response: ‘tolerance’

91
Q

what are the three outcomes after a response

A

RESOLUTION: no tissue damage, macrophages phagocytose debris
REPAIR: healing with scar tissue and regeneration. fibroblasts and collagen synthesis
CHRONIC INFLAMMATION: active inflammation and attempts to repair the damage ongoing

92
Q

What classes of CD4 Thelper cells are there

A

Th1- IL-12 is pro inflammatory helps activate macrophages and cytotoxic cells, TNF, IF gamma
Th2- is pro allergic, Il-4,5,13 and helps to activate B cells
Tfh is pro antibody IL-21, are in B cell zone and help them produce antibody
Treg anti-inflammatory IL-10 TGF beta
th17- pro inflammatory control bacrerual and fungal infection IL17,23,6

93
Q

how are B cells

A

POM (7 decks)

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