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Mechanisms of Microbial Disease > Chapter 1 > Flashcards

Chapter 1 Flashcards

1
Q

What are the two types of the immune system?

A

Innate, which you are born with and adaptive, which is acquired.

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2
Q

What is the innate immune system?

A

The immune system with which you are born. It has no memory and will not improve the resistance with repeated contact.
Limits the entry of pathogens into the body and limits growth.
Skin, lysozyme, complement, c-reactive proteins.
Uses phagocytes and natural cell killers.

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3
Q

What is the adaptive immune system?

A

The immune system that you acquire by encountering pathogens throughout your life. It has memory and will remember a pathogen if you encounter it again in life.
Uses antibodies and T lymphocytes.

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4
Q

Briefly, how does the immune system work?

A

The infectious agent will first encounter the innate immune system. If the innate system cannot fight off the agent itself, the adaptive immune system will come into play to produce recovery and a specific immunologic memory which will stop the agent next time it is encountered. The next time the response will be a faster, better and bigger response.

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5
Q

What is lysozyme?

A

An enzyme found in bodily secretions such as spit and tears that has antimicrobial properties.
Breaks down the peptidoglycan of gram positive bacteria.

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6
Q

What is C-Reactive Protein?

A

A protein that is released in response to inflammation. Coats the surface of dead or dying cells and bacteria.

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7
Q

What is the difference between gram negative and gram positive bacteria?

A

Gram positive bacteria have thick peptidoglycan layers around the cell membrane which causes them to stain purple.
Gram negative bacteria lack the peptidoglycan and stain pink.

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8
Q

What are some biochemical defenses against pathogen entry into the body?

A

Lysozyme in bodily secretions, sebaceous glad secretions, commensal organisms (natural microflora) in the gut and vagina and spermine in semen.

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9
Q

What are some chemical and physical defenses against pathogen entry into the body?

A

Mucus, cilia lining in the trachea, acid in the stomach and skin.

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10
Q

How does penicillin work?

A

It inhibits the synthesis of peptidoglycan in cells, stopping them from being created. Works well because humans don’t usually have gram positive bacteria.

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11
Q

How do bodily membranes limit entry of pathogens?

A

Cilia action to brush up and remove microbes
Secretion of mucus to inhibit bacterial adherence.
Bodily secretions (tears, urine, saliva) protect epithelial surfaces.
Antimicrobial compounds (gastric juice, zinc and spermine in semen, lactoperoxidase in milk, lysozyme)

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12
Q

How do normal flora limit entry of pathogens?

A

These are bacteria and fungi which are permanent residents on the body surfaces and suppress the growth of pathogenic microbes by:
Forming a protective layer
Competing for nutrients
Producing inhibitory compounds (acids, colicins)

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13
Q

How does the innate immune system limit normal growth of pathogens?

A

Phagocytosis and soluble chemical factors (bactericial enzymes)

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14
Q

Who performs phagocytosis?

A

Phagocytes (macrophages and polymorphonuclear granulocytes)

Polymorphonuclear granulocytes are also known as neutrophils and polymorphs.

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15
Q

How are macrophages formed and where are they found?

A

Macrophages are concentrated in the lung, liver and lining of lymph nodes.
Promonocytes in bone marrow become circulating blood monocytes which become mature macrophages in the tissues.

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16
Q

What are neutrophils or polymorphs?

A

The dominant white blood cell in the bloodstream.
No mitochondria, relies only on glycogen stores for energy.
Non-dividing, short-lived, segmented nucleus and granular cytoplasm.
Good diagnostic tool for infection.

17
Q

What are PAMPs?

A

Pathogen Associated Molecular Patterns, which are found on the surfaces of the microbe. Can be composed of LPS or proteins.
PRRs on phagocyte attach and recognize pathogen.
Microbe may sometimes get rid of PAMP to disguise itself.

18
Q

What are PRRs?

A

Pathogen Recognition Receptors which are found on the phagocyte.

19
Q

What happens after the pathogen is recognized by the phagocyte?

A

The pathogen is sucked into the phagocyte using an actin-myosin contractile system and a vacuum is created to form a phagosome.

20
Q

Why is the vacuum in the phagosome important?

A

So the phagocyte does not digest itself while it is digesting the pathogen.

21
Q

What happens to a phagosome?

A

The pathogen is then killed (oxygen dependent or independent or reactive nitrogen species) and the degraded microbe is released outside.

22
Q

How do cationic peptides destroy a cell?

A

Bind to cell membrane and dislodge the cations or poke holes in it.

23
Q

What is the complement system?

A

Cascade in which formyl methionyl peptides that coat pathogens and give off a weak signal to attract leukocytes (chemotaxis).
Contact-dependent.

24
Q

What is C3?

A

The most abundant and central component of the complement system.

25
Q

What does a cascade allow for?

A

More control over the immune system

26
Q

How does the complement system work in normal plasma?

A

C3 is activated and breaks down to C3b and C3a

C3b will complex with factor B to become C3bBb (C3 convertase) which can split more C3

27
Q

What is the stability of C3 convertase like?

A

It is unstable and degrades typically. But in the presence of CHO/other bacterial surface molecule, it is stabilized.
This begins the alternate complement pathway.

28
Q

How does the alternative complement pathway work?

A

Occurs in the presence of bacteria, C3 convertase does not degrade.
C3b binds to the microbial surface and acts as ‘opsonin’ (coating)
C3b and C3 convertase split C5 into C5a and C5b
C5b becomes membrane bound and joined by C6, C7, C8 and C9, forming the membrane attack complex (MAC)
Enhances the rate of phagocytosis.

29
Q

What does C5 do?

A

Gives vasodilation by increasing blood vessel permeability to bring more phagocytes to the site.

30
Q

What is the membrane attack complex (MAC)?

A

Inserts into the lipid layer of the membrane beside C5b and forms a pore, allowing for the leakage of intracellular content.
Can form without C6-9 but not C5.

31
Q

What do C5a and C3a cause?

A

Mast cell degranulation which releases chemicals that mediate:
Increased vascular/capillary permeability
Chemotactic attraction of polymorphs through blood vessel walls to C3b-coated bacteria which bind and phagocytosis occurs

32
Q

How does increased vascular/capillary permeability help fight the infection?

A

Allows the flow of fluid and plasma components to the site of infection.
Part of the “acute inflammatory response”.

33
Q

What are acute phase proteins?

A

Increase in concentration in the plasma in response to injury and inflammation.
Ex: C-Reactive Proteins

34
Q

What are C-Reactive Proteins?

A

The same thing as Mannose binding protein (MBL). Binds to PAMPs and fixes complement and opsonizes bacteria
Good diagnostic tool

35
Q

What are antimicrobial factors?

A

Act within phagocytic cells and body fluids.
Ex: Lysozyme in tears and saliva
Lactoferrin in blood

36
Q

How does lactoferrin work?

A

Binds to free iron in our body, keeping nutrition away from the pathogens.
Indirect killing.

37
Q

What are interferons (IFNs)?

A

Secreted by infected cells and bind to specific receptors on nearby uninfected cells.
It causes the cells to produce 2 types of enzymes that interfere with virus replication to limit spread.

38
Q

What are natural killer cells (NK)?

A

Bind to receptors on virus-infected cells (host) causing NK activation and the release of granules like perforin which form pores in the cell membrane.
Allow the entry of granzyme B that leads to apoptosis.

39
Q

What are eosinophils?

A 
Combat parasites (worms or helminths) that are too big to be engulfed by phagocytes.
Bind to C3b, which causes activation and releases several toxic compounds that damage the cell membrane via hole formation.

Mechanisms of Microbial Disease (17 decks)

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