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Immunology and Infection Flashcards

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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
describe how the spleen filters pathogens and from where
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.
26
What is the epithelial barrier
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
27
Within the gut there are specialised secondary lymphoid tissues called what
peyers patches, below epithelium of small intestine. Are follicles enriched with B cells, lots of germinal centres
28
what are germinal centres
where B cells undergo mutation and selection to make high affinity antibodies
29
The tonsils make what ring
waldeyer ring which have lots of germinal centres
30
how do lymphocytes circulate, if the T cell is far from an antigen what happens
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
31
what is extravasation of naive t cells
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
32
what would happen if there was a wound in the skin
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
33
What is prontosil
bacteriostatic- Gram + sulphonamide antibiotic UTIS- targets folic acid synthesis
34
What is linezolid
targets positive bacterias 50S rRNA subunit to stop protein synthesis bacteriostatic
35
what is daptomycin
bactericidal | targets gram + cell membrane
36
what are macrolides
+ and - 50S subunit targeted stops amino acyl tranfer bacteriostatic
37
what is an antibiotic
antimicrobial agent produced by a microorganism to kill or inhibit other microorganisms
38
what is antimicrobial, antiseptic, bacteriocidal and bacteriostatic
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
what does antibiotic resistance cause
``` increased time for effective therapy additional approached needed expensive therapy aka IV more toxic drugs less effective antibiotics ```
40
what are aminoglycosides
gentamicin, streptomycin bactericidal target protein synthesis, affect 30S subunit to alter RNA proofreading and cause damage to cell membrane
41
what is rifampicin
bacteriacidal RpoB subunit or RNA polymerase to stop transcription red/orange faeces
42
what is vancomycin
bacteriacidal | targets lipid II component of cell wall, crosslinks via d-alanine residues
43
how do beta lactams work
interfere with synthesis of petidoglycan component of cell wall which kills them. bind to penicillin binding proteins
44
what is selective toxicity
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
what are quinolones
synthetic broad spectrum bacteriacidal DNA gyrase in gram -, topoisomerase in gram +
46
what is resistance
if resistant strains can grow above the clinical breakpoint (minimal inhibitory concentration is the lowest concentration of AB's required to inhibit growth)
47
how is antibiotic resistance driven
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
through what four mechanisms does antibiotic resistance occur
1) altered target site 2) inactivation of antibiotic 3) altered metabolism 4) decreased drug accumulation
49
examples of altered target sites
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
examples of antibiotic being inactivated
enzymatic degradation or alteration beta-lactamase ESBL and NDM-1 are broad spectrum beta lactamases
51
what is altered metabolism and examples
increased production of enzyme substrate so it out competes for AB inhibitor inc PABA stops sulfonamides or bacteria switch to other metabolic pathways
52
what is decreased drug accumulation
reduced penetration of Ab into bacterial cell OR increased efflux of AB out so drug cant reach concentration
53
source of AB resistant genes
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
how do AB resistant genes spread from their sources
1) TRANSFORMATION: uptake extracellular DNA 2) CONJUGATION: share plasmid between two bacteria 3) TRANSDUCTION: phages share the DNA
55
why mechanisms of resistance treatment may be hard
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
reasons for tratment failure
``` wrong gram + or - choice AB cant penetrate target site Inappropriate dose due to half lifes Inappropriate administration AB resistance ```
57
risk factors of hospital acquired infection
``` 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
how to reduce resistance
``` 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
How does a gram stain work and what would a purple stain mean vs a pink stain
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
Culture test - haemolysis only works on what bacteria and what does it show
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
what is a lactose test and what type of bacteria is it used on
gram negative If bacteria is lactose fermenting produces lactic acid making the colonies pink, if its a non fermenter will be colourless
62
catalase test is used on what types of bacteria and what does it do
positive catalase positive bacteria will produce bubbles and means its staphlococci catalase negative will produce no bubbles and be streptococci
63
coagulase test is used on what and what does it show
gram positive, checks if can form coagulase | if clumps form its positive and is staph aureus
64
What is the difference in how b and T cells recognise antigens
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
how does clonal expansion occur
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
how is antigen diversity generated
recombination | immunoglobulin gene rearrangement: each BCR chain is encoded by separate multigene families on different chromosomes
67
describe the t cell receptor
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
what is the role of MHC
defining self and not cell, presents antigens | is critical in donor matching
69
difference between MHCI and MHCII
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
what is MHC encoded by, and describe
``` HLA genes. 3 class I and class II loci co dominant maternal and paternal ```
71
what type of T cells react with MHCI and MHCII, what do they look for
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
How do CD4 cells fight infection
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
How do CD8 cell fight infection
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
what is the antibody structure
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
What are the three ways antibodies can work
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
differences between IgG, IgM, IgA, IgD, IgE
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
what does the unique binding site of the B bind to
antigenic determinant aka EPITOPE
78
Naive antigen specific lymphocytes need what to activate them, how do the different activation pathways change the antibody
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
How is thymus independent and thymus independent activation different
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
what is immune regulation and why is it needed
control of immune response to stop inappropriate reactions | needed to avoid excessive lymphocyte activation and tissue damage, prevent inappropriate reactions against self antigen
81
what are the causes of a failing immune regulation
autoimmune disorders allergy hypercytokinemia and cepsis
82
What is autoimmunity
immune response against self antigen.
83
examples and features of autoimmune diseases
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
autoimmunity can be caused by
immune responses against self = autoimmunity, against microbial antigens = crohns immune response inappropriately directed or controlled t cells and antibodies mayc ause self perpetuating
85
allergy is another failure of immune regulation what happens
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
what happens in hypercytokinemia and sepsis
too much immune response, positive feedback loop, pathogens enter wrong compartment
87
describe the phases of cell mediated immunity
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
What is self-limitation
the decline of immune responses, happens when the antigen that initiated the response is eliminated. memory cells are the only survivors
89
what is needed to cause a response to infection
antigens must be recognised co-stimulation of b cell cytokine release cell then responds
90
when are active control mechanisms used
if persistent antigen like self antigens, active control mechanisms are used to limit the response: 'tolerance'
91
what are the three outcomes after a response
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
What classes of CD4 Thelper cells are there
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
how are B cells

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