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MELT 1104 > Outcome 4 > Flashcards

Outcome 4 Flashcards

1
Q

define hypersensitivity

A

A state of reactivity to an antigen that is greater than normal. Typically these responses produce damaging and even fatal results. Four types exist.

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2
Q

identify the four classes of hypersensitivity reactions

A

Type I: Immediate IgE-mediated reactions (allergic reactions). Stimulated by the binding of IgE’s Fc region to FcɛRI (high-affinity Fc receptors) on basophils and mast cells. Causes rhinitis, asthma, and anaphylaxis.

Type II: Humoral cytolytic or cytotoxic reactions that occur when IgM or IgG antibodies bind to antigens on the surface of cells, starting the complement cascade, and the destruction of the cell.

Type III: Immune complex reaction, where antigen-IgM or IgG complexes accumulate in circulation and activate the complement cascade.

Type IV: Delayed-type hypersensitivity. Activated TH1 cells release cytokines that cause the accumulation and activation of macrophages, causing local damage.

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3
Q

discuss the phases of hypersensitivity type I

A
  • sensitization: IgE antibody is produced in response to an antigenic stimulus and binds to a specific receptor on mast cells and basophils.
  • activation: When reexposure to the antigen triggers the mast cell and basophils to degranulate.
  • effector: A complex response occurs as a result of the effects of the many inflammatory mediators released by the mast cells.
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4
Q

What is the other name for type I hypersensitivity

A

Allergic reaction

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5
Q

What is the antibody class involved with type I hypersensitivity

A

IgE

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6
Q

What are the effector cells involved with type I hypersensitivity

A

Basophils, mast cells

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7
Q

What is the mechanism of action for type I hypersensitivity

A

Primary exposure: IgE is produced in response to an allergen, and binds to the FcɛRI region on basophils and mast cells.

Secondary exposure: Ag induces cross-linking of IgE bound to mast cells and basophils, causing them to degranulate, and release preformed mediators.

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8
Q

What is the role of Fc receptors for type I hypersensitivity

A

To allow the two IgE antibodies with a multivalent antigen to bind to basophil and mast cells (cross-linking), causing them to degranulate.

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9
Q

which cytokine is required for class switching in type I hypersensitivity

A

IL-4 and IL-13

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10
Q

define atopy

A

Individuals with a predisposition for IgE development following primary exposure to antigens.

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11
Q

discuss the granule content of basophils/mast cells and their effects

A

Releases performed mediators which are Inflammatory mediators released by activated mast cells that cause the symptoms of allergic reactions.

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12
Q

Histamine

A

causes smooth muscle constriction, increased vascular permeability, and the release of stomach acid.

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13
Q

Serotonin

A

Smooth muscle construction, increased vascular permeability.

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14
Q

Chemotactic factors

A

Factors released following the degranulation of mast cells that attract cells to the site of infection.

Eosinophilic chemotactic factors (ECFs): Attract eosinophils.

Platelet-activating factor (PAF): chemotaxis of inflammatory cells. Induces platelets to aggregate and release histamine and serotonin. Rapidly induces shock-like factors.

IL-8: Attracts neutrophils.

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15
Q

Heparin

A

Inhibition of coagulation.

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16
Q

discuss the role of TH2 lymphocytes in Type I

A

To release cytokines that upregulate IgE responses.

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17
Q

discuss the role of anaphylatoxins in type I reactions

A

Initiates non-IgE mediated degranulation.

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18
Q

discuss the role of eosinophil major basic protein

A

has the ability to destroy parasites and is toxic to the respiratory tract epithlium.

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19
Q

major treatment for anaphylactic reactions

A

Epinephrine: Increases cardiac output, and prevents further cell degranulation.

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20
Q

identify common triggers

A

Insect bites, nuts, penicillin, and seafood.

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21
Q

for type II reactions:
list the other name for this reaction

A

cytotoxic hypersensitivity

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22
Q

for type II reactions:
which antibody classes are usually involved

A

IgM or IgG (IgA and IgE are rare to be involved)

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23
Q

three mechanisms involved for type II hypersensitivity

A

Complement-mediated reactions:
Antibodies react will cell membrane self-antigens (generally blood cells).
ABO incompatibility

Antibody-dependent cell-mediated cytotoxicity (ADCC):
Cell apoptosis

Antibody-mediated cellular dysfunction:
Antibodies bind to cell surface receptors that are critical for the functional integrity of the cell, and dysregulation of cell function without causing cell injury or Inflammation.

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24
Q

role of complement in type II

A

Complement activation has two possible outcomes
1. The cell is lysed by the MAC complex
2. The cell is coated with C3b (opsonin) leading to the cell being phagocytosed

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25
Q

role of antibodies/autoantibodies in type II

A

Antibodies will coat the target cell and then bind to an effector cell (NK, macrophage, neutrophils, eosinophils) using its Fc region. Causes apoptosis in the target cell.

Additionally, antibodies are needed to bind to cell surface receptors necessary for cellular function, impairing the cell without cell injury or inflammation

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26
Q

identify common type II conditions

A

HDFN
Myasthenia gravis
Graves disease

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27
Q

for type III reactions:
List the other name for this reaction

A

immune complex hypersensitivity

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28
Q

identify the antibody class usually involved in type III

A

IgG mainly, or IgM

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29
Q

discuss the role of complement in these reactions in type III

A

Complement creates the fragments C3a and C5a

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30
Q

discuss the differences between localized and systemic reactions for type III

A

Systemic: multiple locations within the body are affected.

Localized: Each time the individual is exposed to the antigen, an increasingly severe reaction occurs at the site of infection. Soluble IgG.

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31
Q

identify common conditions of type III

A

Autoimmune diseases:
SLE
Rheumatoid arthritis
Goodpasture’s syndrome

Drug reactions

Infectious diseases:
Post-streptococcal glomerulonephritis
Meningitis
Hepatitis
Mononucleosis
Malaria
Trypanosomiasis

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32
Q

for type IV reactions:
* discuss how this reaction is different from the other 3 types of hypersensitivity reactions

A

These are delayed reactions that occur 24-48 hours after infection for symptoms to occur.

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33
Q

discuss which subset of T cells are involved in type IV

A

TH1 cells and TH17 cells (Cytotoxic t cells are also involved to a lesser extent.)

release proinflammatory cytokines. release cytokines that damage tissues, causing more cytokines to be released in response to the tissue damage.

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34
Q

discuss what occurs in the sensitization stage in type IV

A

This is the first exposure to the antigen, TH1 and TH17 cells are activated and cloned. 1-2 weeks.

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35
Q

discuss what occurs in the elicitation stage in type IV

A

Subsequent exposures to the antigen will cause the T cells to secrete cytokines, mediating the activation and recruitment of antigen-nonspecific inflammatory cells (macrophages, NK cells, CTL, neutrophils, and B cells). 18-48 hours.

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36
Q

discuss contact dermatitis in type IV

A

Occurs when an inflammatory response is initiated when the skin comes in contact with a sensitizing substance. Eczema is the common expression and occurs 48-72 hours after exposure. The allergen is presented to Langerhans cells, which then present the peptide to T cells that express the appropriate TCR. Clonal expansion of TH1 cells begins.

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37
Q

discuss granulomatous hypersensitivity

A

Gronulomes are formed due to a continuous accumulation of macrophages that cannot clear the infection, adhering to each other, and forming a multinucleated giant cell. This walls off the pathogen from the remainder of the body.

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38
Q

discuss the tuberculin test

A

Used to demonstrate if a person has been exposed to M. tuberculosis A purified protein derivative is injected into the skin. If a lesion forms at the site in injection 24-48 hours after the injection, the person was previously exposed to the bacterium.

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39
Q

discuss the role of innate immunity to protect against pathogens

A

The innate immune system contains barriers to prevent pathogens from entering, and surviving within the body. These barriers are the skin and mucous membranes. Additionally, normal flora prevents the colonization of pathogens by competing for attachment sites, and essential nutrients, or by producing antimicrobial substances.

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40
Q

define the pathogenicity

A

Capacity of a microbe to cause damage to a host.

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41
Q

define virulence

A

The degree of pathogenicity.

42
Q

define susceptibility

A

Degree to which a host is prone to disease.

43
Q

differentiate between the term infection and disease

A

Infection is the acquisition of a microbe by a host, whereas disease is when the infection causes the impairment of the immune system of the host and results in host damage.

44
Q

list and describe the five outcomes of infection

A

Elimination: Interaction of the microbe and the host is not established

Commensalism: Microbe establishes in the host to obtain nutrients and other benefits from the host without causing damage.

Colonization: Microbes that have significant pathogenic potential that establishes within the host without causing symptoms - can still stimulate an immune response.

Persistence: Microbes take up residence in the host, but the immune system is unable to eradicate them despite host damage occurring

Disease: Impairment of the immune system in a susceptible host that results in host damage, and symptoms.

45
Q

list the factors that influence pathogenicity and/or susceptibility

A

Properties of the pathogen (virulence, dose, route of entry)

The ability of the host to resist infection

Breaches in physical barriers/injury

Antimicrobials/immunosuppressive therapy

46
Q

discuss/define opportunistic pathogens/infections

A

These are commensals that become pathogens when host defenses are breached.

47
Q

list the four steps in the infection process

A

adherence/attachment/colonization by the pathogen

Penetration of tissue

Resistance toward host defences allowing colonization and proliferation

Damage to host tissue by pathogens’ virulence

48
Q

discuss host susceptibility

A

Age
health/underlying diseases
Nutritional status
Dosage

49
Q

list common virulence factors used by pathogens and describe their function/role during infection

A

Toxins - destroy host cells

Capsules - resist phagocytosis

Superantigens - bind non-specifically to MHC II molecules, causing T cell activation

Vesicle Formation - Creates membrane-enclosed vesicle with cell impeding MHC binding and peptide presentation.

Enzymes - Destroys polysaccharide that holds the cell together allowing the pathogen to spread through tissue.

50
Q

explain the role of the immune system to protect against bacterial infections

A

Innate, adaptive, Humoral and cell-mediated immune responses.

Innate- phagocytosis, complement, ADCC, and physical barriers.

Adaptive:
Antibody production (TH2- mediated response - extracellular)
T-cell mediated response (TH1- mediated response - intracellular)

51
Q

discuss mechanisms that bacteria use to evade the immune system

A

Secretion of IgA proteases, antigenic variation of attachment pili to avoid IgA antibodies.

Secretion of enzymes to inactivate C3a and C5a. Prevention of MAC insertion.

Uptake of secreted exotoxin into host cells to avoid antibody.

Cell wall endotoxins activate macrophages which release cytokines to cause septic shock damaging host cells.

52
Q

Discuss bacterial types and Effective Responses

A

Gram positive
Extracellular: opsonization and phagocytosis
Intracellular: T cell-mediated and macrophages

Gram negative
Extracellular: complement mediated lysis
Intracellular: T cell-mediated and macrophages

Mycobacteria
T cell-mediated and macrophages

Spirochetes
Complement, antibodies, and T cell-mediated

53
Q

explain the role of the immune system to protect against viral infections

A

Innate immunity uses interferons and complement to slow replication. Adaptive immunity produces antibodies (IgG, and IgA) against the virus. Cytotoxic T cells. Adaptive immunity is required for eliminating the infection.

54
Q

discuss mechanisms that viruses use to evade the immune system

A

Block production of interferons

Secretes IFN receptor homolog that binds to and neutralizes INF-a and INF-b.

Disrupts immune cell migration to the site of infection.

Inhibits MAC

Blocks MHC I transport to the cell surface, decreasing MHC I expression

Interferes with MHC II processing

55
Q

role of antigenic drift/shift in viral infections

A

Antigenic drift
Spontaneous point mutations that occur during replication that introduce minor changes to HA and NA proteins

Antigenic shift
Sudden emergence of a new influenza subtype or strain caused by re-assortment of an entire ssRNA between virions, HA and NA are dramatically different.

56
Q

Oncogenic virus vs Latent form

A

Oncogenic - Able to alter the nucleic acid of the host cell. Host cell becomes a tumor cell

Latent - Viral genome is integrated and carried in host cell DNA following initial infection. Viruses can be reactivated .

57
Q

explain the role of the immune system to protect against parasitic infections

A

Both innate and adaptive mechanisms are needed.

Protozoans
Humoral responses effective against extracellular stages
Cell Mediated immunity effective against intracellular stages

Helminths (worms)
Humoral is the primary response - IgE antibodies
TH2 cytokines

58
Q

discuss mechanisms that parasites use to evade the immune system

A

Physical protective mechanisms:
- Thick extracellular surface that protects from toxic effects of the IR
- Loose surface coats that sloughs off under immune attack

Inhibit complement

Resist phagocytic mechanisms to kill
ingested organisms

Avoid antigen recognition by host
- Alteration of surface glycoprotein antigens
- Host-derived coat that masks parasitic antigens

59
Q

explain the role of the immune system to protect against fungal infections

A

The innate immune system provides primary protection against fungal infection via physical barriers and normal flora.

Cell-mediated immunity is required to eliminate a fungal infection (TH1/ TH17 neutrophils, eosinophils, and macrophages)

60
Q

discuss mechanisms that fungi use to evade the immune system

A

Cell wall is resistant to complement

Acidification of the phagolysosome

Capsule production inhibits phagocytosis

61
Q

describe the pathogenesis of prions

A

Caused by the misfolding of a protein (normal host glycoprotein). This misfolded protein will causes surrounding proteins to misfold, and accumulate in the brain forming plaques.

62
Q

explain the role of the immune system in prion disease

A

No substantial immune response is generated.

63
Q

define what constitutes an emerging and a re-emerging pathogen

A

Emerging - A disease that has appeared in a population for the first time, or that has existed previously but is rapidly increasing in incidence of geographic range.

Re-emerging - diseases that constituted significant health problems in a particular geographic area or globally during a previous time period that declined but now again are becoming health problems of major importance.

64
Q

discuss human behavioral changes in society that have provided opportunities for these pathogens to emerge/re-emerge

A

International mobility/travel

Crowing of poorer population

Crowing of animals and humans

Lapses of public health measures - reduced vaccination

Increased immunodeficient populations

Destruction or invasion of previously
uninhabited or sparsely inhabited ecosystems

65
Q

for Mycobacterium tuberculosis:
* discuss possibilities for the re-emergence of this pathogen

A

Increase in immunocompromised individuals
Crowding of populations
Antibiotic resistance

66
Q

for Mycobacterium tuberculosis:
* explain the role of the immune system to protect against this infection

A

Innate and adaptive immune responses are needed. Granuloma formation can occur in latent TB.

Innate - Airway epithelial cells secrete pro-inflammatory cytokines, macrophages, neutrophils

Adaptive - Involve TH1, and CTLS

67
Q

discuss mechanisms that M. tuberculosis uses to evade the immune system

A

Impairs phagolysosomal fusion
Impairs pro-inflammatory intracellular signaling in macrophages
Impairs NADPH oxidase
Impair antigen presentation
Mycolic acid cell wall is impermeable

68
Q

for SARS-CoV:
* explain the role of the immune system to protect against this infection

A

Cell-mediated:
Innate
IFN, PRRs, NK cells

Adaptive
TH1, CTLS

69
Q

discuss mechanisms that SARS-CoV uses to evade the immune system

A

Antagonize IFN production
- Block mRNA translation
- Degrade mRNA

Modify its viral RNA cap to prevent host detection

Antagonize IFN signaling
- Block intracellular signaling proteins

70
Q

for Ebola virus:
* explain the role of the immune system to protect against this infection

A

Innate: IFN, PRRs, NK, Myeloid cells

Adaptive - required for clearance in humans
Cell mediated: Th1, TH2, CTLs
Humoral: IgG

71
Q

discuss mechanisms that Ebola virus uses to evade the immune system

A

Interferes with IFN production in signaling. Allows rapid dissemination of the virus.

72
Q

Infectious dose vs. Lethal dose

A

Infectious dose refers to the dose of a pathogen that will infect 50% of a population within a specified time.

Lethal dose refers to the dose of pathogen needed to kill 50% of a population within a specified time period.

As the ID50 or LD 50 increases, more of the pathogen is needed for infection.

73
Q

Discuss Zika

A

Associated Guillain-barre syndrome
Causes microcephaly in fetus
Transmission from mother-to-child, sexually, or via mosquitos

74
Q

Discuss COVID-19

A

Virus is transmitted through droplets generated when an infected person coughs, sneezes or exhales.

75
Q

Discuss Monkeypox Virus

A

Relative to the smallpox virus
Major spread is via high risk sexual activity

76
Q

Define pathogenicity island (PAI):

A

Distinct genetic elements on the chromosomes of a large number of bacterial pathogens - encode virulence factors.

77
Q

discuss the principles of immunization and basic mechanisms of protection

A

Active
-Provide the individual with-lasting immunological protection against disease
-Induction of immunity after exposure to an antigen

Passive
- Short-term immunity obtained from the transfer of preformed antibodies
- Recipient’s immune system is not activated towards the antigen of interest
- No memory is acquired

78
Q

extinction

A

specific infectious agent no longer exists in nature or in the lab

79
Q

eradication

A

Permanent reduction to zero of worldwide incidence of an infection by an infectious agent

80
Q

elimination

A

Reduction to zero of the incidence of infection caused by a specific agent in a defined geographical area as a result of deliberate effort

81
Q

control

A

Reduction of disease, prevalence, morbidity or mortality to a locally acceptable level as a result of deliberate efforts

82
Q

discuss the concept of herd immunity

A

Form of indirect protection where if a sufficient percentage of the population is immune to an infection, it reduces the likelihood of infection in individuals who lack immunity. The level of herd immunity varies from pathogen to pathogen based on many factors, but most importantly the reproductive number (R0)

83
Q

discuss the reproductive number of a pathogen and its relationship to herd immunity thresholds

A

The average number of transmission expected from a single primary case into a totally susceptible population. The higher the R0 the more transmissible the virus and the higher need for vaccination. <1 = increase of cases.

84
Q

discuss the principles of eradicability

A

Effective intervention method must exist to interrupt transmission

Sensitive lab tests to detect the levels of infection involved in transmission

Humans are the only host

Zoonotic pathogens are nearly impossible to eradicate due to the animal reservoirs that harbors the pathogen.
All strategies would be directed towards human to human transfer

Unable to amplify in the environment

85
Q

passive vs active

A

Active immunization is immunity after the exposure to an antigen, it takes weeks to build up, but provides long term immunity and immunological memory.

Passive immunity is immunity gained from the transfer of antibodies. It only provides short term immunity, and does not create immunological memory.

86
Q

artificial vs natural

A

Artificial immunization refers to vaccine administration, or passive immunoglobulin therapy. IE. Medical intervention required.

Natural immunization refers to immunity gained from maternal transfer of antibodies, or acquiring the infection.

87
Q

provide examples of each type of immunization

A

Passive/natural: Breastfeeding

Passive/artificial: Immunoglobulin therapy after exposure to HBV in an unvaccinated individual

Active/natural: Acquiring a cold

Active/Artificial: Smallpox vaccine

88
Q

describe the characteristics of an ideal vaccine

A

Safe, and causes minimal side effects

Provides lifelong protection against a disease when given at birth

Easy to administer

Cheap

Stable and easy to transport and store

89
Q

live attenuated

A

Contains whole weakened bacteria or viruses that are able to replicate within the vaccine recipient.
This allows for a strong immune response, and fewer doses of the vaccine are needed for immunity.
In some individuals, the vaccine can cause the disease it is designed to protect against.
Specific storage/transport requirements are needed

90
Q

inactivated/killed

A

Contain whole bacteria or viruses that are inactivated by heat or chemical means, because the pathogen is killed it is unable to replicate within the vaccine host. And the vaccine cannot cause the disease it is designed to protect against.
Boosters are generally required
Does not produce a good IgA response

91
Q

Subunit/fractionated

A

Specific, purified macromolecules derived from a pathogen are used.
Incapable of causing disease, multiple doses are required

92
Q

DNA vaccines

A

Plasmids of DNA that are injected into a vaccine recipient resulting in the production of a pathogen antigen that is encoded on the DNA.
The pathogen protein may be displayed on the surface of the cell as well as presented on MHC molecules.
Incapable of causing disease as there is no infectious agent.
Can be applied to a larger range of pathogens (fungi and parasites)
Potential for the introduction of foreign DNA into the body, and for the immune system to develop tolerance toward the introduced protein

93
Q

mRNA vaccines

A

mRNA for a pathogen is injected into the vaccine recipient.
Cells at the site of injection take up the vaccine and the mRNA is translated in cell cytoplasm to produce the pathogen protein which will be displayed on the surface of the cell as well as presented on MHC molecules

94
Q

route of administration

A

Intramuscular and cutaneous give the best immune response, where orally produces tolerance, and mucous membranes generally cause allergic responses.

95
Q

vaccine type

A

Live attenuated induces a significantly stronger and sustained antibody/cell-mediated response. Non-live vaccines require adjuvants and boosters to generate high and sustained antibody responses. Cell mediated responses tend to be lower in non-live vaccines

96
Q

individual health factors

A

Patients’ immune status can affect why vaccines are able to be given. Often live attenuated are dangerous for severely immunocompromised individuals to receive as the vaccine is more easily able to cause the disease in the vaccine host.

97
Q

Age/timing of vaccination

A

Neonate immunization is deferred to 2 months of age, as administration at birth can cause tolerance or fail to induce a response (exception is HBV). At birth the neonate also still have maternal antibodies in their system, which can interfere with immune response.

98
Q

dose of antigen/type of antigen

A

Higher the dose, the better the immune response. Protein antigens induce better immune responses than polysaccharides.

99
Q

discuss situations where passive immunization would be considered

A

Post-exposure in individuals with no prior immunity to the disease. Immunocompromised individuals. Rh- mothers.
Exposure to: toxins, venoms

100
Q

passive immunization

A

If antibodies are derived from an animal source, the receipt can mount an immune response against the antibodies
Can cause systemic anaphylaxis due to the ingredients used during the preparation.
Can activate complement

101
Q

active immunization

A

Potential to cause disease
Can harm fetuses
Cause side effects
Local hypersensitivity reactions

102
Q

Define Anamnestic response

A

Immune response that leads to a rapid increase in response after re-exposure to an antigen due to the development of immunological memory upon primary exposure

MELT 1104 (5 decks)

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