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HSS1100 - Microbiology & Immunology > Lecture 2 > Flashcards

Lecture 2 Flashcards

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1
Q

What is immunity ?

A
  • The protection against infectious disease granted either by the immune response generated by immunization or previous infection OR by other nonimmunologic factors

Basically… the body’s ability to resist infection from pathogens

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2
Q

Immunity can sometimes be ___________

A

unwated

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3
Q

Immunity can also be ____________, because it has ______________

A

trained, memory

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4
Q

What constitutes non-specific immunity ?

A
  • Natural, innate – Meaning its ALWAYS THERE within us
  • No memory, non-trainable
  • Front line of defence, will be the first to try & protect us against any invader

Will always try to do the same thing first no matter the disease … If doesnt work you need specific immunity

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5
Q

What are the body defences that make part of non-specific immunity ?

A
  • Skin
  • Mucous membranes
  • Iron-binding proteins
  • Phagocytosis
  • Complement
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6
Q

Skin - Non-specific Immunity

A
  • Dry – Pathogens thrive in moist environments, cannot survive in most cases
  • Acidic pH – Sebaceous secretions & sweat contain unsaturated fatty acids (bactericidal)
  • Lower temp – Not ideal for some bacteria
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7
Q

Mucous Membranes - Non-specific Immunity

A
  • Cilia of respiratory tract – Eliminate particles larger than 5 microns (eg. large bacteria carrying dust particles)
  • Lysozymes – Antibacterial substance (eg. in tears)
  • Acidic pH – gastric juice, vagina, urine
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8
Q

Iron-binding proteins - Non-specific Immunity

A

eg. transferrin, lactoferrin

Prevent bacterial growth as iron is a requirement for that in some bacteria

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9
Q

Phagocytosis - Non-specific Immunity

A

Polymorphonuclear WBCs, monocytes, & fixed macrophages in the tissues engulf and eventually destroy bacteria

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10
Q

Complement - Non-specific Immunity

A
  • Set of circulating proteins in blood
  • Opsonization – Binds to antibodies & makes whatever antibodies bound to more attractive for your immune system
  • Membrane Attack Complex [ MAC ] – Able to recognize certain things on bacteria cell walls (eg. sugars) & can come together to form a pore → Allowing insides to leak out → Bacteria dies
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11
Q

What constitutes specific immunity ?

A
  • Acquired, adaptive
  • Directed against 1 particular species of microorganism and not any other
  • Dependent on past exposure (vaccinations)
  • Can be trained to increase strength

Mechanisms aimed at particular infecting organisms are divided into 2 major systems :
- Specific circulating antibodies in body fluids [ humoral immunity ]
- Cells trained to attack specific invading organisms [ cell mediated immunity ]

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12
Q

What are the immune cells ?

A

B cells – Make antibodies
T helper 1 & 2 cells – Mediators that signal which type of specific immune response we need to deploy (humoral / cell mediated)
- TH1 → Controls cell-mediated immunity
- TH2 → Controls humoural response

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13
Q

What is humoral immunity ?

A

The presence of circulating antibodies which are modified serum globulins tailored to react with particular chemical components of previously encountered invading organisms

Produced ONLY in response to these encounters

  • EXTRACELLULAR PATHOGENS – Plays an important role in infections in which the pathogen produces toxins or has a capsule, as well as some viral infections

B cells are lights in a room, TH2 light switch
- TH2 cells turn on B cells via binding (tells it to start making more antibodies in response to the pathogen)

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14
Q

What are antibodies (Ab) ?

A

Referred to as immunoglobulin (Ig) , made in response to stimulation by an antigen & reacting specifically with it

Synthesized by B-lymphocytes / B-cells (plasma cells), production process requires antigen-presenting cells & T-helper 2 + T suppressor cells

  • Able to distinguish foreign macromolecules (NON-SELF) from ‘normal’ body constituents (SELF)
  • Recognize toxins, capsules & some viral proteins
  • High specificity in combination with antigens
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15
Q

Antibodies : Constant vs Variable Region

A

Constant Region – Identical in all antibodies of the same isotype
- Determines mechanism used to destroy antigen

Variable Region – Responsible for antigen recognition, what actually BINDS to the antigen
- Each B cell makes a unique antibody that recognizes the antigen

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16
Q

What are the 5 classes of immunoglobulins ?

A

IgG, IgA, IgM, IgE & IgD

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17
Q

Which of the immunoglobins involved in defence mechanisms ?

A

IgG, IgA & IgM

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18
Q

IgG

A
  • Basic unit found is a Y-shaped molecule
  • Has 2 sites that combine specifically with the antigens, like a key in a lock
  • The rest of the molecule can bind phagocytes and macrophages, which eventually destroy the microorganism
  • Crosses placenta to later protect newborn
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19
Q

IgA

A
  • Found in secretions (eg. mucosae of the respiratory, gastrointestinal & genito urinary tract, tears, milk, etc)
  • Dimer : Made of 2 joined units of wide molecules to keep constant together
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20
Q

IgM

A

FIRST ANTIBODY THAT IS MADE + Main 1 produced in the early immune response
- Pentamer : Made of 5 units joined together
- Does NOT cross the placenta

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21
Q

IgE

A
  • Involved in some hypersensitivity states
  • Can lead to allergies if too many are made
  • Defends against parasites
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22
Q

IgD

A

Role not completely understood
- VERY low levels in blood
- May have role in parasite function

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23
Q

What are antigens (Ag) ?

A

The chemical components which stimulate the production of antibodies which are then able to react specifically with those antigens

Capable of inducing a specific immune response - both humoral (production of Ab) & cell-mediated

Must be recognized by body as foreign (“non-self”) otherwise auto-immune disease can result
&
Antigenic structures in pathogen must be UNIQUE / not be found inside of you

  • Usu protein, but can be glycoprotein, lipoprotein, polysaccharide
  • Can be particulate or soluble
  • Mol weight must be at least 10,000 to trigger an immune response
  • Bacterial cells contain a number of antigenic molecules – Capsular substance, flagella, cell wall, etc.
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24
Q

Viruses usu have ______________ antigens

A

polypeptide

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25
Q

___ arms of the antibody bind to antigen

A

Y

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26
Q

Agglutinations

A

Antibodies can bind to another pathogen (of the same type) & clump it together
- Keeps pathogen localized / constrained so the body can efficiently get rid of it

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27
Q

The Primary Immune Response

A
  • First intro of an antigen into the body triggers the production of Ab against the foreign substance
  • Lag (latent) period for up to several days
  • Circulating antibodies detectable in 5 - 10 days
  • Serum antibody peaks at about 3 weeks / 21 days then level drops (eventually to undetectable levels)

Vaccines are PRIMARY

28
Q

The Secondary Immune Response

A

Occurs when an antigen is introduced for the 2nd, 3rd, 4th time, etc. [ BASIS FOR IMMUNIZATIONS !!! ]

  • After a short lag, the titer of antibody rises rapidly (2-3 days)
  • Then slowly decreases over a much longer period, stabilizing at a lower level
  • May be repeated several times until antibody level reaches a maximum usually after 3 - 5 injections of antigen

Booster injections are SECONDARY

  • Not always equally efficient for everyone
  • Different mutations / variations pose challenges (eg. common cold evolves often)
29
Q

The Serological Reaction

A

Used to detect presence of antibodies in a serum sample (eg. screening of blood donors)

  • Agglutination – Usual result demonstrating an observable antigen-antibody reaction
    “clumping”
  • Titration of Ab – Permits quantitation of antibody in patient sera

Unknown microorganisms can be identified with known diagnostic antisera

30
Q

What is cell mediated immunity ?

A
  • The basic mechanism is similar to that of humoral immunity in that exposure to an antigen induces production of “trained” cells active against that antigen or any organism that carries it. The main difference is that soluble antibodies are NOT involved
  • Helper, suppressive, cytotoxic (killer) cells generated from memory (trained) T-cells / T-helper 1

Occurs inside CELL rather than blood → Ab cannot get through so we need TH1 to destroy cell or localize pathogen & destroy it inside the cell

TH1 is active in most microbial infections & is essential in the defense against :
INTRACELLULAR PATHOGENS
Some viruses
Parasites
Tumor cells
Foreign cells (grafts, transplants)

Immune-suppressive medication for transplant recipients

31
Q

Stages of Lymphocyte Functions

A
  • II – Antigen processing by macrophage and presentation to lymphocytes; assistance to B cells by T cells
  • IIIB & IIIT – Lymphocyte activation, clonal expansion and formation of memory B and T cells
  • IV – Humoral immunity, B-cell line produces antibodies to react with the original antigen
  • V – Cell-mediated immunity, Activated T cells perform various functions on the original antigen
32
Q

What are Antigen-Presenting Cells ?

A

Group of immune cells that help mediate the response upon exposure to an antigen

  • Will take in the antigen & prepare to display (present) it on its surface & binds with special receptors on T-helper cells (TH1 or TH2 depending on immune response required)
  • Response is directed by chemicals (interleukin, etc)
  • Receptors are either MHC1 or MHC2 (major histocompatibility complexes)
  • Presentation depends on how antigen is viewed
    ( Intra vs extracellular )
33
Q

Pathway of Specific Immune Response

A
  1. Pathogens eaten up by macrophages from lymph nodes
  2. APC displays portion of pathogen on surface
  3. Helper T-cells recognize pathogen & are activated

TH1 activates cytotoxic T-cell
1 pathway → Kills infected cells
2 pathway → Becomes memory T-cell

TH2 activates B-cell
1 pathway → Becomes memory B-cell
2 pathway → Becomes plasma cell
Forms ANTIBODIES

  • Sometimes the APC does not do a good job bc pathogen is too virulent / can kill you
  • Vaccines present a solution (same thing as natural immunity but you only get part of the pathogen so that it is not fatal)
34
Q

The immune system is NOT perfect …

A
35
Q

Disorders of Immunity

A

*4 situations in which the immune system can be harmful to its host : *

  • Allergy & hypersensitivity states – Overreaction to antigens, in the absence of infection (can be fatal, with airway obstruction + circulatory collapse → ANAPHYLAXIS)
    Such reaction can be observed when administering vaccines to individuals who are allergic to a component of the vaccine, such as traces of egg proteins, etc.
  • Auto-immune diseases – The immune system of some individuals can react to its own “SELF” antigens, including the formation of auto-antibodies (Ab against yourself)
    – eg. Type 1 diabetes, MS, rheumatoid arthritis, lupus
  • Immunodeficiency states – Some individuals lack the ability of producing antibodies, cell-mediated immunity or both ( Can be the result of congenital abnormalities, irradiation or disease, such as AIDS )
  • Graft rejection (kidney, bone-marrow, heart, etc) – In transplanted patients, the rejection of the graft is a NORMAL reaction of the immune system, which recognizes the foreign grafted organ as “non-self”
  • But this is harmful to the patient and has to be controlled by immuno-suppressive drugs (then makes you at risk for disease)
36
Q

Matching transplants must not have …

A

antigens that host doesn’t have

37
Q

Passive Immunization

A

Administration of preformed antibody (IgG) against a specific microbial agent, usually by the intramuscular route
- The preformed antibody is obtained from humans or derived from animals, usually horses, which have been actively immunized against the particular microbial agent
- No need to do primary immune response & will never do secondary

When might you want to do it ? If you need the quick-administeration of short-term (temporary) protection or if you are breastfeeding

Gamma globulin (IgG): pooled from large grouped of blood donors and has antibodies to many common infections
Hyperimmune globulins (IgG): specific for a particular microbe

38
Q

IgG of animal origin :

A
  • Recognized as foreign by the immune system & cleared from the recipient in about 10 days (short-lived)
  • Carries the risk of hypersensitivity reactions (IgE antibodies) such as serum sickness & anaphylaxis
39
Q

IgG of human origin :

A
  • Also disappears from the circulation after several weeks (also short-lived)
  • Does NOT carry the risk of hypersensitivity reactions
40
Q

Active Immunization

A
  • Stimulation of the body’s immune mechanisms through administration of a vaccine = an antigen = an immunogen from a microbial agent
  • Longer-lasting than passive immunization → Gain a primary immune response
  • “Better”
41
Q

Live-Attenuated Vaccines

A

Generally result in a subclinical or mild illness that duplicates the disease to be prevented
- Usu provide both local (IgA) & humoral immunity (IgG)
- Rapid immunity development than with killed vaccines
- Serious illness from the vaccine itself can result in immuno-compromised individuals

42
Q

Killed-Vaccines, subunits & toxoids

A

Antigens without infectivity
- Killed antigen remains shape
- May need boosters for secondary response
- Toxoids administered in presence of an adjuvant

43
Q

Recombinant Vaccines

A

Produced by DNA recombinant technology, which avoids the possibility of a live virus surviving the inactivation process
- Weakens / attenuates microorganism

Best-known example is hepatitis B vaccine

44
Q

Hepatitis B is a ____________ vaccine

A

recombinant

45
Q

Adsorbed Vaccines (aD not aB)

A

Vaccines mixed with inorganic salts, more slowly adsorbed by the tissues –> Provides lasting immunity

  • Stays in circulation longer to allow antigen presenting cell to find it
  • Tetanus & diphtheria
46
Q

Conjugate Vaccines

A
  • Designed for poorly antigenic microorganisms
  • Conjugate (bind) antigen of interest to immunogenic, non-toxic protein (will make APC recognize pathogen)

Hemophilus influenzae type b

47
Q

What is Combined Active-Passive Immunization ?

A

If potentially exposed to a pathogen, u can be injected with passive immunization for immediate protection as well as active immunization

  • Several live attenuated vaccines or several killed vaccines, subunits vaccines & toxoids can be combined together to facilitate their administration
  • Hyperimmune Igs & vaccine injected at DIFFERENT sites so they don’t cancel eachother out and cause agglutination
48
Q

What is Penicillin ?

A

First antibiotic, discovered in 1929 by Sir Alexander Fleming
- Used in WWII to treat staphylococcui & streptococci (1946)

Resistance recognized almost immediately → 80 % of all staphylococcus aureus

Still used to treat streptococcus pyogenes (Group A strep)

Has NEVER been effective against gm-negatives (salmonella, shigella, bordetella pertussis, etc) bc their cell walls are surrounded by a lipopolysaccharide (LPS) layer that prevents antibiotic entry into cell

49
Q

Antibiotics in early 1940s & 1950s

A
50
Q

Current Circumstances of Antibiotic Resistance

A
51
Q

Antibiotic Resistance

A
  • With current overuse & overprescribing of antibiotics, we are forcing bacteria to change (evolve) in order to survive
  • Bacteria will develop resistance to virtually any antibiotic given sufficient time :

Resistance occurs when a susceptible microorganism is no longer inhibited by an antibiotic agent

52
Q

Intrinsic Resistance

A
  • Predictable form of resistance, based on the mechanism(s) of action of the antibiotic & the characteristics of the microorganisms
  • Characteristics of microorganism vis-avis antibiotics mechanism of action
53
Q

Extrinsic Resistance

A
  • Previously susceptible organism becoming resistant to an antibiotic’s action
  • New or added

Driven by 2 genetic processes :
- Mutation & selection (vertical evolution)
- Exchange of genetic material (horizontal evolution)

This type is clinically more important & involves 3 main mechanisms of resistance :
- Alteration in drug target
- Production of inactivating enzymes
- Decreased antibiotic uptake

54
Q

Alteration of Drug Target

A
  • Antibiotic gets inside bacteria + attaches to circular enzyme → Enzyme doesn’t work, bacteria dies
  • Some bacteria will change enzyme from circle to square so that antibiotic no longer binds, but square shape still functional
  • Wherever antibiotic binds, it will cause it to change shape
55
Q

Production of Inactivating Enzymes

A

Some bacteria will produce an enzyme that will modify the antibiotic → Rendering it useless

56
Q

Decreased Uptake of Antibiotic

A

Occurs in 1 of 2 ways :
Cell wall becomes less permeable (antibiotic no longer able to come in)
Turns on efflux proteins → Binds to antibiotic as it comes in & throws it out

57
Q

Genetics of Antibiotic Resistance

A
58
Q

Antibiotic genes may confer resistance by :

A
59
Q

Exchange of Genetic Material - Conjugation (plasmid(

A
60
Q

Exchange of Genetic Material - Transformation

A
61
Q

Exchange of Genetic Material - Transduction

A
62
Q

Exchange of Genetic Material - Transposition

A
63
Q

Chromosomal Alteration or Activation

A
64
Q

Mar

A

multiple drug resistance

65
Q

Decreasing Antibiotic Resistance

A
66
Q

Antibiotic Therapy

A
67
Q

Viruses usu have ______________ antigens

A

polypeptide

HSS1100 - Microbiology & Immunology (4 decks)

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