2.3 - Infection and Defects in Mechanisms of Defence Flashcards

1
Q

6 Factors Influencing Infection

A

1) Communicability
- how easily a pathogen can spread from 1 person to another
ex. HIV has low communicability bc it requires specific transmission routes

2) Infectivity
- ability of pathogen to invade and multiply within a host
- involves attachment to cell surface, enzyme release, and spread through lymph

3) Virulence
- severity of disease a pathogen can cause
ex.rabies - causes severe and fatal disease

4) Pathogenicity
- ability to produce disease
- depends on combination of virulence, communicability, and infectivity

5) Portal of Entry
- route by which pathogen infects the host
- direct, inhalation, ingestion, bites

6) Toxigenicity
- ability to produce toxins
- more effective a pathogen is at producing toxins, the more severe disease it can cause

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2
Q

Bacterial Disease

A

How Bacteria produces toxins
1) Exotoxins
- enzymes that damage host cell directly (damage membrane or interfere w protein synthesis)

2) Endotoxins
- get released into the bloodstream activate the inflammatory response

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3
Q

What is Bacteremia/Septicemia?

A

Bacteremia: the presence of bacteria in blood
Septicemia: growth of bacteria in blood

  • failure of the body’s defence mechanism
  • when this happens, endotoxins get released and activate complement/clotting system - increases permeability; allows plasma and bacteria to leak into tissue
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4
Q

Viral Disease

A
  • most common
  • usually resolves on its own
  • transmits through: infect blood, sexual contact, aerosol, and vectors (moving things)
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5
Q

How do viruses replicate?

A
  • viruses NEED A HOST to replicate

1) Attach - binds to receptor

2) Penetrate - fuses with membrane

3) Uncoat - viral material is released from protective coat

4) Replicate - viral material replicates to make viral proteins

5) Assemble - viral proteins assemble into particles

6) Release - new virions are released

  • some viruses remain latent until triggered by something
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6
Q

How Virus affects Host Cell

A

1) inhibits DNA, RNA, synthesis in hist cell (bc virus is producing its own virions)

2) Breaks lysosomes
- digestive enzymes get released and damage the cell

3) Can cause cancer
- viruses can cause uncontrollable growth = cancer

4) Make the virus more susceptible to infections
- virus impairs immune response

5) Viral cells can fuse and disrupt tissue structure/function

6) Viruses change surface proteins on cell
- not recognized by immune system; so gets attacked

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7
Q

What is Antigenic Variation

A
  • minor gradual changes in antigens overtime
  • virus cumulates mutations and leads to new strains
    ex. different variants of COVID, influenza
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8
Q

Fungal Infection

A
  • fungi are large microorganisms without peptidoglycans; makes them resistant to antibiotics

Dermatophytes: fungi that invade skin, hair, and nails

  • fungi adapt to their host environment and suppress the immune defence
    • they can adapt bc they can tolerate wide range of conditions: low O2
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9
Q

Parasitic Infection

A
  • parasites live symbiotically within a host

Spread through
- human to human via vectors (mosquitos)
- contaminated food and water

  • parasites cause damage by sitting in the space alone (not by causing immune response)
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10
Q

Purpose of Antimicrobials

A
  • drugs used to kill/stop growth of microbes
  • inhibit synthesis of cell wall
  • damage membrane
  • alter metabolism (ability to process RNA)
  • inhibits protein synthesis
  • modifies metabolism (bacteria can not produce energy)
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11
Q

How does bacteria develop resistance?

A

1) Mutations
- mutations can make them resistant

2) Inactivate antibiotic
- some bacteria produce enzymes that neutralize antibiotics

3) Modify target molecule

4) Antibiotic Efflux
- bacteria can pump the antibiotic out faster than it can enter

5) Lack of compliance to antibiotic regime
- if you do not complete prescribed course, 1 bacteria can be left alive and replicate

6) Overuse
- overusing antibiotics can also kill beneficial bacteria - resistant bacteria thrives bc healthy bacteria does not compete with it

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12
Q

How do Vaccines work?

A
  • vaccines stimulate the immune system without causing the disease
  • helps the body to make memory cells that trigger a mire immediate response upon exposure
  • vaccines use weakened or dead pathogens
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13
Q

What is an Immune Deficiency

A
  • failure of the immune systems defence mechanisms

Classified as:
Primary (congenital)
- occurs from genetic anomalies at birth
- inherited defects in the immune system
- rare and often undiganosed

Secondary
- obtained over time
- caused by another factor

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14
Q

What are combined deficiencies?

A
  • result from underdevelopment of B and T lymphocytes

1) Severe Combined Immunodeficiency
- absent IgM and IgA
- underdeveloped thymus
- few lymphocytes

2) Bare lymphocyte syndrome
- B and T cells can not properly present

3) Wiskott - Aldrich
- low IgM increases susceptibility to infections

4) DiGeorge Syndrome
- diminished parathyroid development

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15
Q

Evaluation of Immune System Function

A

1) Complete Blood Count
- tells us about circulating blood cells and amount of lymphocytes

2) Quantitative determinant of Immunoglobulins
- measures level of antibodies

3) Assay
- checks the complement system

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16
Q

What is Hypersensitivity?

A
  • altered immune response to antigen that results in disease or damage to host

Immediate Rxn
- causes anaphylaxis

Delayed Reaction
1) Allergen
- hypersensitivity to environmental antigen

2) Autoimmunity
- immune system mistankenly targets its own tissues

2) Alloimmunity
- reaction to tissues from another person

17
Q

Type I Hypersensitivity

A
  • IgE antibodies are triggered in response to environmental antigen
  • 1st exposure: IgE binds to mast cells
    -Re-exposure: allergens binds to IgE on mast cells
  • causes mast cell degranulation which releases histamine
  • histamine acts on H1 and H2 receptors = allergy symptoms
  • Symptoms: itching, swelling, mucous production, runny nose, sneezing

Anti-histamines - block histamine from binding and alleviate allergy symptoms

18
Q

Type II Hypersensitivity

A

Tissue: specific - tissue is the target of an immune response

Mechanisms
1) Antibodies bind to cell and mark it for destruction

2) Phagocytosis: macrophages engulf and destroy marked cells

3) Antigens enter circulation or deposit on tissues (destroys tissues)

4) Antibodies bind to target cells and recruit other immune cells that causes cells to malfunction

Ex. Graves disease - antibodies target thyroid to produce too many proteins

19
Q

Type III Hypersensitivity

A
  • formation of antigen-antibody complexes in the bloodstream
  • complexes deposit in tissues or blood vessels
  • when immune system recognizes the deposit, it releases lysosomal enxymes to break it down
  • this triggers widespread inflammation
  • NOT ORGAN SPECIFIC
20
Q

Type IV Hypersensitivity

A
  • does NOT involve antibodies
  • relies o T cells either to
    1) directly kill cells OR
    2) recruit other immune cells

ex. Graft rejection - immune system recognizes foreign transplant and attacks it

21
Q

What is an Allergy?

A
  • most common hypersensitivity
  • triggered by environmental antigens that the immune system mistakenly attacks bc it thinks its foreign
  • allergen is contained with a particle that is too large top be phagocytosed
22
Q

What is Anaphylaxis?

A
  • most rapid and severe hypersensitivity reaction
  • can be systemic or affecting specific areas
  • severe reactions can lead to shock and death

How to Reduce
- Desensitization: gradually exposing a patient to increasing amount of allergen so they become sensitized

23
Q

Systemic Lupus Erythematosus

A
  • chronic, multi-system inflammatory disease
  • immune system produces antibodies that attack the bodies own components
  • forms antigen-antibody complexes that depsosit in tissues
24
Q

Alloimmunity

A
  • occurs when a blood types does not match recipient blood type
  • blood types are determined by the antigens on the surface of RBC’s

Ex. RH
- RH + - have Rh antigens
- RH - - no rh antigens
- if mother is rh - but baby is Rh +, RH _ will pass to mother whp recognizes it as foregn and produced anti-TH antibodies
- in next pregnancy, if baby is RH +, anti-rh antibodies can cross placenta and attack fetal RBC;s