immunology Flashcards
1
Q
Clinica infection
A
Infections with signs and symptoms
2
Q
Subclinical infection
A
Infection with pathogen but no symptoms
3
Q
Localised infection
A
Confined to one area of body
4
Q
Systemic infection
A
Spread to different areas of body
5
Q
Iatrogenic (nosocomial) infection
A
From a medical practitioner / intervention (hospital)
6
Q
Exogenous infection
A
from external environment
7
Q
Endogenous
A
From within the human host
Congenital disease is a type of endogenous (from mother to fetus)
8
Q
modes of disease transmission
A
- Contact transmission(direct & indirect physical contact)
- Common vehicle transmission (air-borne, food- & water-borne)
- Vectors (mechanical & biological)
- Direct inoculation (parenteral)
- Intra-placental
contact by droplet blood and wounds sexual trans oral-faecal route respiratory-salivary route zoonoses
9
Q
Reservoirs of Infectious Agents + e.g
A
Animate (carriers)
• healthy
•. active disease
• convalescent
Inanimate eg. air, dust, soil, food etc.
10
Q
epidemiology
A
The study of the spread, frequency, distribution of disease
– Specific source
– Factors determining spread
11
Q
epidemiology types
A
• Descriptive epidemiology
– Data relating to location, ages, time, occupation, etc to track disease
• Analytical epidemiology
– Disease in detail to identify cause, transmission and prevention
12
Q
classifications of disease
A
endemic
epidemic
pandemic
sporadic
13
Q
Endemic
A
Disease present in a community (region) all the time, usually only clinical in a few
14
Q
Epidemic
A
Wide spread disease within a community (region), affecting many people but only occasionally present
15
Q
Pandemic
A
Wide spread epidemic, not confined to a single community or region (more than one continent)
16
Q
Sporadic
A
Widely scattered disease, occurring singly, irregularly, infrequently
17
Q
Aetiology
A
Cause of the disease
18
Q
Outbreak of Infection
A
Occurrence of number of cases of disease over the expected in a given time & place
19
Q
Morbidity
A
Number made ill by infective agent
20
Q
Mortality
A
Number of deaths caused by infective agent
21
Q
Incidence
A
Number of new cases over specific period
22
Q
Prevalence
A
Number of cases (infected or diseased) at a given time (old and new cases)
23
Q
first epi study
A
• Dr John Snow (1813 – 1858), investigated a cholera outbreak in London in 1854
• Mapped cases which centered around a water pump on Broad street
– water was thought to be curative by locals
• Had the handle removed and well blocked
• Sewage was contaminating water
• Stopped outbreak!
• Bacterial cause of cholera was unknown at the time.
24
Q
how to control epidemic disease
A
- Prevent contamination of water supplies
- Proper treatment of water supplies
- Proper sewage treatment and disposal
- Immunization
- Health personnel and community workers
- Educate the public
- Eliminate reservoirs of infection
- isolate diseased persons
- immunization programs
- treat sick persons
SARS good example of successful controls used to prevent spread of disease
25
factors influencing the disease spread
• Virulence of the pathogen
• Pathogen transmission mode
• Population susceptibility
– Immunity
26
immune system is and does
Loose collection of cells, tissues, proteins and organs widely distributed throughout the body
– Homeostatic mechanism
– Surveillance (detect changes)
– Discriminate between self and non-self
– Destroy non-self (defend against attack)
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immune system response type and description
• Innate:
– Non specific defences which do not require previous exposure to foreign agent
• Adaptive:
– Response based on specific recognition of invader (foreign agent)
• Antibody mediated (humoral)
• Cell mediated
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non specific innate defence types
Inflammation – complex response to tissue injury (vasodilation, cytokines, coagulation, attraction & adhesion of WBC - fever from pyrogens)
Phagocytosis – engulfing and destroying invaders NK cells
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specific adaptive defense types
– B- lymphocytes – antibody production
| – T-lymphocytes – help antibody production, cell mediated cytotoxicity
30
inflammation response + effects and signs
Response to injury
– Trauma, chemical, infection, heat
• Effects
– Prevents spread
– Removal of debris / infectious agent – Repair
• Four “Cardinal signs”
– Redness, heat, swelling, pain,
• limitation of joint movement (if joint involved)
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inflammatory chemical released
Release of chemicals mediators
(from damaged cells and resident Mast cells)
* Histamine, complement, kinins, prostaglandins
* Release of Leukotactic (chemotactic) agents
* Leukocytosis inducing factor
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chemical mediators what do
• Increase vaso-dialation
– Increase blood to area
• Increaseoxygen,nutrients,temperature
• Increasemetabolicrateofcells
• HeatandRedness
• Increase capillary permeability
– Capillaries leak fluid
• Proteinfluidintotissuespaces
• Clottingfactors,complement,(antibodies)
• Clot forms a barrier prevents spread
• Painandswelling
33
innate non-specific defences - first line defense
Mechanical barriers
intact mucous membrane
intact skin
Normal flora
Competition
```
Secretions
Mechanical removal and Germicidal
action Sebum (oil) pH 5
antimicrobial peptides
Acid in gastric juice
Spermine and zinc in semen
Lactoperoxidase in milk
Lysozyme in tears, nasal secretions and saliva
```
Mucus in digestive and respiratory tracts
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innate non-specific defence - second line
Serum
– Complement, a series of 20 proteins, adhere, initiate inflammation, kill cells
• membrane lesions by attaching to bacterial cells directly or via antibodies
– Other anti-microbial peptides
• Interferon
• acute phase proteins
White Blood Cells (leucocytes)
– Phagocytic
• Neutrophils, monocytes + eosinophils are (eosinophils also destroy large parasites)
• Basophils (mast cells) release inflammatory chemicals
– Natural killer cells (NK)
35
Antigen Presenting Cells - APC
* Professional antigen presenting cells move around detecting foreign antigens
* Phagocytose infectious invader (antigen)
* Digest and present bits of antigen on its surface travel to local lymphnode
* Present antigen to T-helper cells
* T-h then stimulates adaptive immune response
36
lymphocytes cells and the immune system they involved in
```
t cells (adaptive)
b cells (adaptive)
NK cells (innate and adaptive)
```
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t cells
(adaptive)
• Cytotoxic T cells (T-C), T helper (T-H), T regulator (T-reg)
• 80% of lymphocytes
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B cells
(adaptive)
• Ig on surface, become plasma cells to produce antibody
• 15% of lymphocytes
39
NK cells
(innate and adaptive)
• Natural killer cells (Kill virus infected cells and cancer cells)
• 5% of lymphocytes
40
T cell types
T-h
T-reg
T-c
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T-h
– Detect antigen on antigen presenting cells
– Activate macrophages, Tc and B cells
– Stimulates adaptive immune response
42
T-reg
Suppress the immune response
43
T-c
Cytotoxic T cells that kill virus infected cells and cancer cells
44
Adaptive immunity
Adaptive immunity fight invaders once innate system breached
• More specific than innate system
• Has memory
• Mediated by lymphocytes
45
Adaptive immunity division
Divided into two, although there is overlap and communication
1. Humoral Immunity
2. Cell Mediated Immunity (CMI)
46
Humoral Immunity
• Antibody mediated immunity
• Antibodies made by B cells (turn into plasma cells)
• Antibodies are specialised proteins that recognise and attach to antigen
• Recognise antigen on a foreign invader
– Antibodies stick to antigen
Action against extracellular invader
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Antibodies
* Belong to Immunoglobulin group of proteins
* They have two heavy and two light chains linked by disulfide bonds
* Constant region and two variable region (end of Y shape)
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Antigens
* Antigens stimulate the generation of antibodies
* Antibodies have specific binding (variable region) regions to specific antigens
* Foreign objects have proteins, carbohydrates that act as antigens.
49
Epitopes or Antigenic determinants are
Specific region on antigens where Antibodies bind
50
Primary response
* Initial exposure to antigen stimulates a primary humoral response
* Primary response has a lag of several days while B cells proliferate (time for invader to do harm)
* Antibody levels peaks and falls as antigen is removed
* The type of antibody is IgM (Immunoglobulin M)
51
secondary response
* Second exposure to the same antigen stimulates the secondary immune response
* The response is much quicker and larger with a rapid rise in antibody levels
* Lasts longer
* Memory cells require fewer cycles to become plasma cells (shorter reaction time)
• The antibody type is IgG (Immunoglobulin G)
52
Cell Mediated Immunity
Lymphocytes directly / indirectly kill infected cells
Act against intracellular invaders (also cancer)
• Humoral immunity only effective against extracellular antigen
• Viruses and mycobacteria are intracellular infections (out of reach of humoral response)
• Cancer cells also need to be removed
• The mechanism for protection against these attacks is the Cell Mediated Immune (CMI) response
• Two populations of T cells involved:
– Cytotoxic T cells (TC)
– Natural Killer cells (NK cells)
53
Cytotoxic T-cells (Tc)
• Wide range of surface receptors against antigen called T cell receptors (TCR)
• Each TC is specific for one receptor
• Infected cells express the antigen (of the invader) on their surface
• TC via T cell receptor binds and destroys cells expressing the specific antigen
• Kill by release of toxic molecules
– effect membrane causing lysis,
– initiate apoptosis
54
Natural Killer cells
• Natural Killer cells (NK cells) recognise reduced MHC 1 (protein on surface of cells) and kill the cell
– Cancer cells and many virus infected cells have reduced MHC 1
• NK cells kill by Antibody Dependant Cell Cytotoxicity (ADCC)
– NK cells have receptors that recognise antibodies
– Can bind and kill cells that have antibodies on them
• Killing is similar to TC cells – release of cytotoxic molecules
55
Regulation of immune response
• The activation of B and Tc cells is regulated by T lymphocytes (T cells)
– T helper cells (TH) stimulate
– T regulator cells (TReg) inhibit
– TH specific for the antigen stimulate B cells to proliferate to plasma cells producing antibody, once antigen removed TReg inhibit TH and stop production
56
Passive immunity
– Rely on administration of antibodies (already directed against an antigen)
– Often after infection or toxin
– The recipient does not produce an immune response of their own
– Short term
57
active immunity
– Administration of antigen
– Prophylaxis (prevent future infection)
– The recipient mounts a response producing own antibodies and memory
– Long term
58
Autoimmune disease (what, who)
• When Immune system attacks self.
– Antigen on a microbe similar to self antigen
– T cells and antibodies made against microbe cross react with self
Who:
Mostly western society - women - adults
Genetic component?
Insulin Dependent Diabetes Mellitus (IDDM)
– Type 1
– Destruction of the β-cells of islets of langerhans in pancreas
– β-cells responsible for insulin production
– Cytotoxic T cells followed by auto-antibodies
– Anti-Islet cell antibodies (ICA)
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