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Immunology and healthcare > Theme 3 & 4: Vaccination & healthcare > Flashcards

Theme 3 & 4: Vaccination & healthcare Flashcards

1
Q

2 main functions of a vaccine. What can be measured to see the effectiveness of a vaccine

A

-Vaccination protects you against the pathogen, as well as conserves your immunity you already have, against other infections

  • Antibody level in the serum
  • T cell production
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2
Q

Function of memory B cells and T cells

A
  • memorize the characteristics of the antigen during initial infection so in secondary infections, it triggers an accelerated and stronger immune response, where IgG predominates.
  • Memory B cells -faster antibody production. Class switched Ig
  • this memory is long lasting and maintained in the absence of antigen
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3
Q

How was small pox eradicated (1979)

A
  • Cowpox and smallpox viruses share some surface antigens
  • So injecting people with cowpox induced antibody production which could also be used to neutralise the smallpox virus

-This strategy doesn’t work in other cases unfortunately

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4
Q

What a vaccine needs to be in order to be effective and practical.

A
  • safe: not cause illness
  • Protective against illness from the pathogen, lasting for several years
  • Induces neutralising antibodies to prevent the pathogen infecting irreplaceable cells
  • Induces protective T cells
  • Practical considerations: low cost, easy storage, few side-effects, easy administration, long shelf life, stable, don’t clump
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5
Q

Explain briefly the main types of vaccines (Vaccines based on killed organisms, based on attenuated organisms, live-attenuated vaccines, recombinant vaccines, RNA vaccines, recombinant viral protein vaccines, Capsular polysaccharide vaccines) Give examples of vaccines/ diseases for each

A
  1. Vaccines attenuated on killed organisms: culture lots of infective organism, then inactivate them using chemicals/ heat/ radiation. It still has their antigens but unable to replicate. (eg. flu vaccine)
  2. live-attenuated organisms: cultured virus inserted into non-human cells, so no longer replicates in human cells, but body recognises the antigens. Better immune response. Not very effective in adults (eg. BCG for TB)
  3. Recombinant: Insert antigen producing gene into plasmid. Plasmid infects yeast and makes lots of proteins which can be extracted and used as a vaccine (HPV, Hep B, meningitis)
  4. RNA vaccines: extract viral RNA, put in lipid coat. -80C storage. (SARS CoV2, as it removes the spike proteins)
  5. Recombinant viral protein vaccines: make spike proteins in lab. Elicits immune response when injected. (Covid)
  6. Capsular polysaccharide vaccines: Need for conjugation to toxin to be effective in all patients
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6
Q

What are adjuvants used for in vaccines. What substance can be used for this.
What 4 other elements are in the vaccine formulation

A
  • Substances added to vaccine to encourage sterile inflammation, because the pathogen alone may not elicit a good innate response
    eg. aluminium salts
  • Preservatives
  • Stabalizers (prevent chemical reactions)
  • Surfactants (prevent clumping)
  • Dilutent (sterile water)
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7
Q

What is passive immunisation

A
  • person receives antibodies or lymphocytes that have been produced by another individual’s immune system
  • occurs naturally from mother to foetus, during development, breast feeding (IgA), across placenta (IgG).
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8
Q

Why passive immunity is important for a baby

A
  • mother’s immune cells and Ig genes transferred to baby

- this is essential because it takes time for a baby’s immune system to fully develop (6 months after birth)

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9
Q

What is herd immunity and how is it achieved

A
  • Herd immunity established when a significant amount of the population is vaccinated
  • If the majority of the population are protected then the susceptible minority are protected, as low probability of pathogen finding these people.
  • infection harder to spread
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10
Q

Are diphtheria, polio and measles eradicated

A

-No, although vaccination has been successful and so very low incidence

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11
Q

Measles: transmission, symptoms, severe complications

A
  • Droplets in coughs and sneezes
  • sneezing, runny nose, fever, tiredness, aching, loss of appetite, diarrhoea, conjunctivitis, spots merging to blotches, Koplik’s spots in mouth

virus infects leukocytes, suppressing immunity
-Severe complications: Encephalitis, meningitis, febrile convulsions, pneumonia, hepatitis, damage to hearing, death.

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12
Q

What is social demography

A
  • The relationships between economic, social, cultural, and biological processes influencing a population
  • these challenges affect the implementation of vaccines
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13
Q

When was widespread vaccination introduced, how many vaccines are there now

A
  • 1950s

- vaccines against 26 infectious diseases

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14
Q

Why is the HIV and malaria vaccine so hard to develop

A
  • Malaria is a challenging vaccine to develop due to complex life cycle
  • HIV: high mutation rate
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15
Q

What key things are tested for in the 4 stages of clinical trials for vaccines. how many people are involved in each stage

A
  • Phase I (<100 people)= safety and dose
  • Phase II (>100 people)= side effects, if it elicits an immune response, consistency
  • Phase III (>1000 people)= efficacy, safety, rarer side effects.
  • Double blind trial used to compare instance of disease with patients injected with placebo and with the vaccine.

-Phase IV: post marketing surveillance

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16
Q

What affects people’s views on vaccines. Why people are against them

A
  • Given false information about side effects (info spreads fast with social media)
  • Misconseptions of risk: don’t realise that risk from the vaccine are completely outweighed by getting the disease
  • Media tends to focus on the very small studies
  • Fear of needles
  • Cost of getting the vaccine
  • Campaigns: anti-vaxxers
  • Religious and cultural beliefs
  • Mistrust of science, medicine, government, healthcare systems
  • Ignorance of disease- don’t know how fatal it can be
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17
Q

How you would explain what a vaccine is to a patient and why they are important

A
  • Vaccines provide immunity to a particular infectious disease. Protects the individual and also the population as it reduces it spreading
  • The vaccine teaches your body to make antibodies that protect you against the pathogen if you were to become exposed to it
  • It contains a weakened or inactivated microbe, or an agent that resembles its toxins or surface proteins. It elicits an immune response, so that our body has memory and is immune to secondary exposure

-So for example, for covid, the spike proteins on the virus is what allows it to infect human cells. So by creating the protein in a lab, we can inject it into people so that it elicits an immune response and train our body to make antibodies for it, but without any viral replication and infection. The immune response means that our body has memory and immunity to the disease if we were to become exposed to it.

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18
Q

What demographic factors compromise vaccine effectiveness/ implementation

A
  • poor healthcare and low income countries
  • Porous borders, so easily spread
  • Political issues: government not giving out info, loss of trust
  • Ageing and increasingly obese populations so vaccines less effective
  • Isolation of terrorist groups: Don’t take part in healthcare measures so no chance of creating herd immunity
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19
Q

How do we address social demographic issues in vaccination

A
  • Education (about the facts)
  • Campaigns
  • Improved surveillance and vigilance
  • Data in the public domain e.g. genome data
  • Health partnerships between international agencies e.g. UNICEF/WHO and local health ministries
  • Development of innovative funding initiatives
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20
Q

What are the requirements/ aims of a successful tissue and organ transplant

A
  • transplants have to be physiologically viable
  • the process should not harm the recipient
  • transplant should not be rejected by the recipient’s immune system. This is done by giving immunosuppressive drugs to suppress the immune system, and HLA matching.
  • adequate blood supply (to limit ischameia) to avoid inflammation
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21
Q

Difference between hyperacute, acute and chronic rejection during transplantation (type of hypersensitive, how it is caused, give examples)

A
  1. Hyperacute: immediate onset, type II hypersenstivity, caused by pre-existing antibodies on cell surface binding to the graft (non-self HLA) Causes vascular damage. Eg. in pregnancy, multiple blood transfusions, previous transplants.
  2. Acute rejection: type IV hypersensitivity. Mediated by T cells attacking alloantigens/ the transplant. Eg. kidney transplant, bone marrow transplant.
  3. Chronic: type III hypersensitivity. Reaction between antibodies and HLA recruits monocytes and neutrophils and allograft specific T cells
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22
Q

How is transplant rejection avoided

A
  • Matching HLA antigens
  • Immunosupressive drugs before and after surgery

-Otherwise causes graft-versus host disease

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23
Q

What are alloantigens/ alloreactions, and autoantigens/ autoreactions

A
  • Alloantigens: someone else’s antigens, not your own. Alloreaction is an immune response to alloantigens
  • Autoantigens: your own antigens. Immune response to own antigens
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24
Q

What a rejected kidney looks like. What type of rejection is this

A
  • Acutely rejected (type IV hypersensitivity), but may progress to chronic rejection.
  • caused by T cells attacking transplant

-Red areas of haemorrhage, grey areas of necrosis, swollen

25
Q

What is chronic rejection caused by (4 things). And what it leads to

A
  • Type III hypersensitivity
  • Also caused by ischaemic reperfusion injury, viral infection and relapse of original disorder
  • Autooantibodies bind HLA on endothelium transplanted organ, recruiting lots of immune cells
  • Leads to atherosclerosis, hypoperfusion, fibrosis, atrophy and gradual loss of function.
26
Q

What transplants need little and lots of HLA matching

A
  • Cornea transplant= little
  • Then liver, heart and kidney needs increasingly more.
  • Bone marrows highly sensitive to HLA mismatch so high susceptibility to graft v host disease
27
Q

Name the action of the immunosuppressive drugs: corticosteroids, azathioprine, cyclosporin A. Side effects of cyclosporin

A
  • Corticosteroids -inhibit cytokine production by macrophages, reduced exudate fluid in lung tissues.
  • Azathioprine- interfere with DNA synthesis so inhibits lymphocyte proliferation
  • Cyclosporin A -inhibits T cells. But side effects include high BP, inflamed gums, abdominal & back pain
28
Q

What are monoclonal antibodies and their uses.

A
  • Monoclonal = a specific antibody made by cloning a unique white blood cell.
  • used for diagnosis and therapies (biologics for autoimmune diseases)
29
Q

How are monoclonal antibodies produced, (using a mouse)

A
  • Immunise a mouse with an antigen you are interested in
  • Take B cells and fuse them with cancer/ myeloma cells to make a hybridoma so that they are immortal so they can be cultured.
  • Select for antigen-specific hybridoma and genetically modify them so that humans don’t recognise them as foreign.
  • and clone these cells
30
Q

How immunodeficiencies can be diagnosed. (How flow cytometry works, ELISA, immunofluorescence)

A
  • Looking for any absences in immune cells.
  • Ig levels, lymphocyte count
  • Flow cytometry allows you to identify specific cell types and deficiencies
  • Tag cells with a fluorescent and can identify cells with TCR (T cells) and with Ig (B cells) when plotted on a dot plot
  • ELISA can detect autoantibodies and quantify them using spectrophotometer.
  • Immunoflurescence: fluorescently labelled autoantibody to detect antigens. Only can tell if it is present or not.
31
Q

How X linked agammaglobulinaemia is diagnosed using flow cytometry

A
  • Fluorescent will show how many cells have TCR and Ig on their surface so can see how many T and B cells there are
  • The immunodeficiency has a lack of B cells and antibodies. So there will be few dots in the box showing B cells.
32
Q

How are allergies diagnosed. What 3 substances are involved.

A

Intradermal skin test. Inject the following substances:

  1. Suspect antigen (food, chemical, cat hair) Then look for a wheal and flare
  2. Negative control: Saline. No flare should occur here.
  3. Positive control: histamine. Should cause a reaction
33
Q

What cells produce histamine and in what type of hypersensitivity

A
  • involved in Type I

- Mast cells

34
Q

What are biologics and what do they treat.

A
  • Drugs made from proteins and other substances derived from nature.
  • Therapeutic antibodies are either derived from humans/ mice/ genetically engineered.
  • When injected, they bind to antigens/ self antigens, inhibiting the action of proinflammtory cytokines, B cells or T cells to suppress the immune response in autoimmune diseases (Crohn’s, arthritis) or kidney transplantation.
  • Can also be used to treat cancer (eg. eliminating cancerous B cells)
35
Q

How omalizumab treats asthma. What cytokine infliximab inhibits to manage Crohn’s and rheumatoid arthritis

A
  • Omalizumab: removes IgE antibody so mast cells cannot acquire this on its surface so down regulates it. Mast cells are involved in asthma by producing cytokines and proteases.
  • Infliximad: inhibits inflammatory cytokine TNF-a to reduce inflammation.
36
Q

Cancer: benign and malignant definitions

A

-Cancer is caused by inappropriate division of cells. Can either be:
1-Benign: cells contained in fibrous connective tissue so cannot spread
2-Malignant: dysplastic cells that spread and invade.

37
Q

Why immune system is slow at recognising cancers (2 points)

A
  • Cancers are slow growing

- are very similar imunologically to healthy cells

38
Q

why old age increases risk of cancer. (2 points)

A
  • More immunosupressed due to meds, and dysregulated immune systems from deficiencies (zinc). so more susceptible to infections that can lead to cancer.
  • cells become damaged over time. More exposure to radiation for example.
39
Q

3 ways that cancers/mutations can be detected by immune system/ causes an immune response

A
  1. Gene mutations in cell surface proteins make cells unrecognisable so get an immune response
  2. Tumor may express proteins not usually expressed in adult life (embryonic genes). So recognized as non-self.
  3. Over expression of normal self proteins changes self-peptide presentation, so recognised by T cells.
40
Q

Why viruses can lead to disease

A

Viruses interfere with normal mechanisms involved in cell division, causing inappropriate proliferation and transformation of cells, leading to cancer

41
Q

What cancers can HPV, Hep B, Epstein Barr and HIV, HHV8 cause

A
  • Papillomavirus: head & neck. And cervical cancer (99% cervical linked with HPV)
  • Heb: liver cancer
  • Epstein-barr virus (HHV4): Burkitt’s lymphoma
  • HIV: T cell leukaemia
  • HHV8: Kaposi’s sarcoma
42
Q

What bacteria is associated with stomach ulcers and stomach cancers

A

Helicobacter pylori

43
Q

Why HPV can cause cervical cancer

A
  • HPV infects epithelial cells.
  • It inhibits p53. p53 important for inhibiting cyclin dependant kinases so prevents progression through the cell cycle, allowing DNA to be repaired.
  • Therefore its inhibition allows cells to proliferate beyond normal regulatory mechanisms
44
Q

How is Heb B and C transmitted. And consequences of infection

A
  • Blood-borne. Blood and saliva
  • Transmitted via blood contaminated instruments, sexual intercourse, needles, mother to child.

-Heptitis, liver cirrhosis, liver cancer

45
Q

What blood cells does Hep C inhibit. Why we don’t have an effective vaccine for the virus

A
  • Inhibits activation of dendritic cells (APC), which has a knock on effect on T cells
  • And, like heb b, it promotes Treg so supresses immunity

-Mutates rapidly

46
Q

How biologics can help treat cancers

A
  • Monoclonal antibodies target specific antigens:
    1. Target cancer molecules to get rid of them
    2. Boost host immune system
    3. Can identify size and location of the tumor, so know where other therapies need to target
47
Q

Brief description of bone marrow transplants and how it causes graft v host disease

A
  • Radio and chemotherapy kills cancerous blood cells (eg. in leukaemia) and obliterates the bone marrow.
  • Allogenic bone marrow transplant to transplant haematopoietic stem cells to repair the haematopoietic system with non-cancerous blood cells

-T cells from donor can attack recipient tissues as it recognizes them as foreign, causing graft v host disease

48
Q

Elements of the immune response in the mouth (lots)

A
  • epithelium: physical barrier to prevent invasion, mucous layer, keratin, secrete AMPs, desquamation.
  • Saliva: antimicrobials (histatin), IgA, mucin, lysozyme, lactoferrin, agglutinin, peroxidase.
  • GCF: serum exudate. antimicrobials, antibodies
  • Enamel pellicle
  • Commensal bacteria
  • Vascularity
49
Q

Name components of saliva: i) antimicrobials for disrupting membranes ii) adhesive proteins for agglutination in fluid phase, iii) protease inhibitors to remove nutrients. v) metal ion chelators for removing nutrients

A

I) defensins, histatins, statherin, cathelicidin, lysozyme

ii) mucin (MG2), agglutinin, proline rich proteins, gp340
iii) cystatin
v) calprotectin (zinc) and lactoferrin (iron)

50
Q

What cytokine is involved in recruitment of neutrophils

A

IL-8

51
Q

How anatomy differs from intestine, to sulcular & junctional epithelium in mouth. And why these features make periodontitis occur quite easily

A
  1. Bacteria varies greatly, depending on oral hygiene
  2. No mucin in sulcus, thick mucous layer in intestine for a barrier
  3. Intestine has IgA. Sulcus doesn’t so has IgG instead
  4. Epithelial cells in intestine have tight junctions, whereas junctional epithelium is highly porous, so allows easy penetration of pathogens
  5. Intestine has stable physiological inflammation, whereas it is difficult to prevent damaging inflammation in mouth
52
Q

What defences/ molecules are involved the 3 phases in oral immune response: non-induced, innate, adaptive

A
  1. Natural non-induced host defences: Saliva, pellicle, commensals, vascularity, integrity of oral mucosa. [involved in inactivation, clearance, prevention of attachment and invasion]
  2. Innate immunity: GCF [contains and clears infection]
  3. Adaptive: [enhancement of innate, long lasting immunity]
53
Q

What immunoglobulin is in saliva and its function. How is it produced

A
  • IgA
  • Inhibit adherence and penetration by neutralising pathogen. Forms complexes with mucins for bacterial clearance
  • Secreted by saliva glands by plasma cells in response to antigens in the GI tracts after being swallowed.
  • Antigen presented by dendritic cells to T cells. Plasma cells make IgA which is secreted from salivary glands
54
Q

What are the different PAMPS of periodontal pathogens that can be identified by Pattern recognition receptors (eg. Toll like receptors)

A

LPS, proteases, fimbriae, DNA, short chain fatty acids, whole bacteria, lipotechoic acid etc.

55
Q

What is the role of IL-1B in periodontal inflammation

A
  • in small amounts of inflammation, it activates macrophages, neutrophils, dendritic cells. This can remove the pathogen
  • In excess irritation by plaque, they cause fibroblasts to release MMPs which degrade collagen and bone.
56
Q

What vaccine delivery by mucosal route rather than infection

A

polio

Infects the CNS causing paralysis

57
Q

What vaccine is manufactured to contain tetanus toxoid

A

Pneumococcal conjugate vaccine

58
Q

What does the MMR vaccine protect you against

A

measles, mumps, rubella

Immunology and healthcare (4 decks)

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