1
Q
What is immunisation?
A
A process to protect against infection
2
Q
What is vaccination?
A
Vaccination is a very effective ‘type’ of immunisation.
3
Q
How long can vaccine-induced protection last?
A
Protection can be short-term
(~months) or long-lasting (years
to a lifetime).
4
Q
What are the two main types of immunisation?
A
Passive immunisation and Active immunisation.
5
Q
What is passive immunisation?
A
Protection transferred from another person or animal as
antibody or cells – usually short-term
6
Q
What is active immunisation?
A
Protection produced by the person’s own immune system - usually long-lasting
7
Q
How does passive immunisation occur naturally in early life?
A
Through maternal antibody transfer.
8
Q
Which maternal antibody crosses the placenta?
A
IgG, mainly during the third trimester.
9
Q
Which antibodies are transferred via breast milk?
A
IgA > IgM > IgG, especially in colostrum
10
Q
How long does maternal protection last?
A
1-3 months after being born, based on the mother’s immune system.
11
Q
At what point do infants start to produce their own adaptive immune response?
A
After about 3 months of life they’ll start to get their own IgGs.
12
Q
When does infant IgG production reach protective levels?
A
Around the 6-month mark
13
Q
What is artificial passive immunisation?
A
Administration of antibodies or immune cells from another source as a prevention or therapy against infection
14
Q
What is heterologous hyperimmune serum?
A
Serum derived from non-human animals immunised against a specific antigen.
15
Q
What are examples of heterologous serum use?
A
Horse antiserum for rabies or diphtheria toxin treatment in humans
16
Q
What are the risks of heterologous serum therapy?
A
Serum sickness and immune complex hypersensitivity reactions.
17
Q
What is homologous pooled antibody?
A
A preparation of immunoglobulins pooled from the plasma of many healthy human donors.
Antibodies are broad but not specifically concentrated for a certain antigen.
Examples:
IVIG (Intravenous Immunoglobulin)
IM Immunoglobulin (Intramuscular)
18
Q
What is homologous hyperimmune globulin?
A
Collected from human donors with high antibody levels against a specific pathogen; lower risk of serum sickness.
Examples:
Parvovirus immunoglobulin
Varicella zoster immunoglobulin
Hepatitis B immunoglobulin
19
Q
Is immunity from passively administered immunoglobulins long-lasting?
A
No, it is short-lived because no memory cells are generated.
20
Q
When should passive immunisation be given for prophylaxis?
A
Shortly before expected exposure (e.g., before travel to an endemic area).
21
Q
When should passive immunisation be given for therapy?
A
Immediately after suspected exposure (e.g., after a rabid dog bite).
22
Q
How does rabies immune globulin (RIG) work after exposure?
A
Once in tissues at the entry site, rabies virus can be neutralised by passively administered rabies immune globulin (RIG).
23
Q
When should RIG be administered for maximum effectiveness?
A
Immediately after exposure, before symptoms appear.
24
Q
When do virus-neutralising antibodies (VNA) appear after vaccination?
A
Approximately 7–10 days after starting the rabies vaccine series
25
Why is RIG critical in early post-exposure prophylaxis?
Because adaptive immunity takes time to develop, and RIG provides immediate passive protection
26
Why is active immunisation considered the most important public health intervention of the 20th century?
Because it prevents infectious diseases on a large scale
27
How is active immunity produced?
After delivery of a vaccine, which stimulates the body’s own immune system.
28
How does immunity from vaccination compare to natural infection?
It is similar to natural immunity but achieved without the risk of disease.
29
What is the main purpose of vaccination?
To prevent deaths and illness caused by infectious diseases by building immunity in the population
30
Does vaccination completely eliminate disease burden?
No, vaccine-preventable diseases still cause illness and some deaths, though at much lower rates.
31
Name some vaccine-preventable diseases that still impact Australians today.
Influenza, HPV, pneumococcal disease, meningococcal disease, shingles, and whooping cough
32
What is herd immunity?
Indirect protection from infection when a large enough proportion of the community is immune, reducing disease transmission.
33
What vaccination rate is usually needed to achieve herd immunity?
Greater than 90%.
34
Why do we care about herd immunity?
Because not everyone can get immunised, such as immunocompromised people.
35
How does herd immunity help protect people who are not vaccinated?
It reduces the overall transmission of disease, lowering the chance of exposure for unvaccinated individuals.
36
Who received the PCV7 pneumococcal vaccine vaccine when it was introduced?
Children aged 2–5 years
37
What effect did the PCV7 vaccine have on adults?
A reduction in pneumococcal disease was observed in adults, even though they were not vaccinated. Vaccinating children indirectly protected adults.
38
What is R0 (R nought)?
A measure of contagiousness. R0 is the average number of people that will get infected from a single case in an immunologically naïve population
39
What happens if R₀ < 1?
The disease will decline and eventually die out.
40
What happens if R₀ = 1?
Disease will stay alive and stable, but there won’t be an outbreak
41
What happens if R₀ > 1?
If R0 is more than 1, each existing infection causes more than one new infection. The disease will be transmitted between people – may lead to outbreak or epidemic
42
How can measles vaccination reduce mortality from other childhood diseases?
By preventing measles infection, which otherwise causes immunosuppression and increases vulnerability to other infections.
43
What is “immune amnesia” in the context of measles?
A condition where measles infection erases immune memory, reducing B and T cell memory to previously encountered pathogens
44
What is the relationship between measles vaccination rates and mortality from non-measles infections?
Countries with low measles vaccination rates have higher mortality from other infectious diseases.
45
How do vaccines work?
By generating an antigen specific immune response (adaptive immunity)
46
What are the basic components that all vaccines have?
An adjuvant + an antigen.
47
What is an adjuvant and what does it do?
Something that activates the immune system
PAMPs or PAMP-like chemicals
They activate PRRs on
innate cells. If we just put an antigen into someone it might not generate a sufficient immune response without the adjuvant telling it to activate.
48
What is an antigen in relation to the vaccine?
Something specific to the pathogen
49
What can antigens be?
Usually proteins but can be polysaccharides or lipids
50
What does the antigen do?
Stimulate specific B and T cells
51
What are the three main types of vaccines?
Live vaccines
Killed / Inactivated / Component vaccines
‘Constructed’ vaccines
52
What are killed/inactivated/component vaccines?
Vaccines made from killed microorganisms, their virulence factors, or toxins.
53
What are ‘constructed’ vaccines?
Vaccines developed using advanced biotechnology, such as DNA vaccines, Immunostimulating Complexes (ISCOMS), recombinant proteins, mRNA vaccines, and recombinant viruses.
54
What are live (attenuated) vaccines?
Vaccines containing live, weakened forms of the pathogen that can replicate but do not cause disease in healthy individuals.
55
How do live vaccines induce immunity?
They mimic natural infection, inducing strong, long-lasting immune responses, often providing lifelong immunity with one or two doses.
56
What are the advantages of live vaccines?
Robust, durable immunity and may induce both antibody and T cell responses
57
What are the disadvantages of live vaccines?
Not suitable for immunocompromised individuals, may cause mild infection, and require cold storage.
58
Give examples of live (attenuated) vaccines.
Measles, Mumps, Rubella (MMR), Varicella (chickenpox), and oral polio vaccine (OPV).
59
How are attenuated vaccines made?
Serial Passage in Cell Cultures: The pathogen is repeatedly passed through cultures of cells that are not its usual host.
Pathogen accumulates mutations that reduce its ability to thrive in human cells.
60
Give examples of attenuation methods.
OPV: Poliovirus grown in monkey kidney cells
Measles vaccine: Virus grown in chicken eggs
61
What are killed (inactivated) vaccines?
Vaccines containing pathogens that have been killed or inactivated so they cannot replicate but still trigger an immune response.
62
How do killed vaccines stimulate immunity?
They primarily stimulate humoral (antibody) immunity through antigen recognition without causing disease.
63
What are the advantages of killed vaccines?
Safer for immunocompromised individuals, stable and easier to store, with no risk of causing the disease
64
What are the disadvantages of killed vaccines?
May require multiple doses or boosters for long-term immunity; typically induces a weaker immune response compared to live vaccines.
65
Give examples of killed (inactivated) vaccines.
Inactivated polio vaccine (IPV), hepatitis A vaccine, rabies vaccine.
66
How is polio transmitted?
By the faecal-oral route
67
What are common symptoms of polio?
Fever, sore throat, headache, nausea, and fatigue—usually self-resolving
68
What severe complication can polio cause?
Paralytic polio (1–5% of cases), leading to muscle weakness or paralysis, sometimes affecting respiratory muscles.
69
Who developed the two major polio vaccines?
Jonas Salk (IPV – inactivated polio vaccine) and Albert Sabin (OPV – oral polio vaccine).
70
How is the Salk vaccine (IPV) administered?
By intramuscular injection.
71
How does IPV work?
Uses killed poliovirus to trigger an immune response and prevent poliomyelitis.
72
Advantages of IPV?
– Safe for immunocompromised
– No risk of vaccine derived polio
73
Disadvantages of IPV?
– Requires booster doses
– Does not induce mucosal immunity in the gut
74
How is the Sabin vaccine (OPV) administered?
By oral drops.
75
How does OPV work?
Replicates in the gut, providing both systemic and intestinal immunity.
76
Advantages of OPV?
– Induces strong and lasting immunity
– Prevents virus spread by stopping replication in the gut
– Easy to administer, suitable for mass vaccination campaigns
77
Disadvantages of OPV?
– Risk of vaccine-derived polio (occurs approximately 4 in 1,000,000)
– Not recommended for immunocompromised individuals
78
What are constructed vaccines?
Vaccines that contain only specific pieces of the pathogen, such as proteins or genetic material, that trigger an immune response without using the whole virus or bacterium.
79
How are constructed vaccines made?
They use synthetic or genetically engineered components such as recombinant proteins, conjugates, DNA, or mRNA, to stimulate immunity
80
What are the advantages of constructed vaccines?
Highly specific, with reduced risk of adverse reactions; often safer for individuals with weakened immune systems.
81
What are the disadvantages of constructed vaccines?
May require adjuvants to enhance immune response; sometimes need booster shots for sustained immunity.
82
Give an example of a constructed vaccine.
COVID-19 mRNA vaccines (Pfizer, Moderna).
83
What do subunit vaccines use?
Only specific antigens from a pathogen, usually a polysaccharide or protein, not the entire microbe.
84
Why are subunit vaccines considered safe?
They use only parts of the pathogen, leading to very few side effects.
85
What is a major limitation of subunit vaccines?
They are often not very immunogenic and require adjuvants to boost the immune response.
86
Give an example of a subunit vaccine still used today.
Acellular pertussis vaccine.
87
Why can polysaccharides not be presented on MHC molecules?
Because they are sugars, not peptides.
88
What is a recombinant vaccine?
A genetically engineered version of a subunit vaccine where a gene from a pathogen is inserted into a host cell (yeast, bacterium, or mammalian cell) to produce the antigen.
89
What are conjugate vaccines designed to improve?
Immune responses to bacterial polysaccharides.
90
Why do polysaccharides alone elicit a weak immune response?
They trigger a T-cell–independent response, which is less effective and does not create strong memory.
91
How do conjugate vaccines work?
Proteins are chemically linked to polysaccharides, creating a T-cell–dependent response.
92
What is the benefit of linking proteins to polysaccharides in vaccines?
It stimulates strong, long-lasting immunity and immune memory
93
What is a disadvantage of conjugate vaccines?
They are complex and expensive to manufacture.
94
What are the main aims of active immunisation?
To provoke specific immune responses and reduce disease burden.
95
Which immune responses does active immunisation aim to provoke?
Provoke specific:
– Humoral immunity (antibody)
– Cell mediated immunity (T cells)
– Immunological memory (long-term protection) in
both B-cells and T-cells
96
How does active immunisation reduce disease burden?
Reduce disease burden by:
– Preventing initial infection
– Delaying established infection
– Limiting pathogen load and spread
– Reduce disease severity/death
97
What is a correlate of protection?
A measurable immune marker that is statistically associated with protection against infection or disease
98
What is the most common correlate of protection?
Antibody titres.
99
Why are correlates of protection useful?
They help compare vaccine effectiveness and determine what level of immunity is needed for protection.
100
What are the five characteristics of the ideal vaccine?
1. Activates both T and B cells to give class-switched antibodies and memory cells
2. Generates long-lived plasma cells that produce persistent antibody
3. Generates T cells (helper + killer) to several epitopes
4. Results in sterililing immunity, and
5. Does not result in excessive inflammation/adverse events
101
What is the general rule of vaccination regarding immune response?
The more similar a vaccine is to the natural disease, the better the immune response (immunogenicity) and protection.
102
What is the trade-off with stronger immune responses from vaccines?
The stronger the immune response, the greater the chance of adverse reactions (reactogenicity).
103
What are some practicalities of vaccines?
Does the vaccine require multiple doses?
How often is a booster required?
Is it better to target a particular age group?
Safe for pregnant women?
104
Why can some vaccines be expensive?
Complex manufacturing processes, such as for conjugate vaccines, increase costs.
105
What storage conditions do many vaccines require?
Strict cold storage (2–8°C) to maintain efficacy
106
Why is cold storage a challenge in some settings?
Low-resource environments may lack reliable refrigeration.
107
Why is surveillance important after vaccination programs?
To monitor long-term safety and effectiveness.
108
Are safety and efficacy always aligned in vaccine design?
No, they are not always mutual outcomes—designing a vaccine requires balancing both.
109
What is the main challenge in vaccine design?
Achieving strong protection (efficacy) while minimising adverse reactions (safety).
110
How many deaths were averted by measles immunisation between 2000–2021 (WHO)?
56 million deaths.
111
What percentage of children will seroconvert to measles in countries without immunisation programs?
99%
112
Compare risks: What is the rate of death per million doses of MMR vaccine vs per million measles cases?
MMR vaccine: 0.2–3? per million doses
Measles infection: 100–100,000 per million cases
113
Does MMR cause autism?
No, MMR does not cause autism.
114
Why is immunisation sometimes considered a victim of its own success?
Because widespread vaccination reduces disease prevalence, leading to complacency and ignorance about the importance of vaccines.
115
What factors contribute to declining vaccine uptake?
Increasing number of vaccines and complex schedules
Ignorance of scientific basis for immunisation
Underestimation of severity of vaccine-preventable diseases
Growing perception of vaccine dangers
BMS211
flashcards
Decks in class (21)
# Cards
-
Cells and organs of the adaptive immune system5
-
Preformed / Innate Defences25
-
Phase II responses & Local Inflammation32
-
Phase III Responses & Systemic Inflammation20
-
Antigen Presentation and MHC33
-
T cell biology and Thymus32
-
Effector T cells I32
-
Effector T cells II44
-
Antibodies/B cells I103
-
Antibodies/B cells II89
-
T and B cell memory51
-
Extracellular defence101
-
Intracellular defence84
-
Intracellular defence II103
-
Immunisation115
-
Tumour Immunology74
-
Cancer Immunotherapy44
-
Hypersensitivity123
-
Autoimmunity/Tolernance59
-
Transplants/HLA0
-
Immunodeficiency0
