Nonspecific Defenses of the Host Flashcards

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1
Q

List the first line of defense (nonspecific) (3)

A
  1. Intact skin
  2. Mucous membranes and their secretions
  3. Normal mibrobiota
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2
Q

List the second line of defense (nonspecific) (4)

A
  1. Phagocytic WBCs
  2. Inflammation
  3. Fever
  4. Antimicrobial substances
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3
Q

List the third line of defense (specific defense) (2)

A
  1. Specialized lymphocytes B cells and T cells

2. Antibodies

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4
Q

How does epidermis function in the defense of microbial invasion? (3)

A

The Epidermis consists of many layers of continuous sheets of tightly packed epithelial cells w/ little or no material b/w the cells

a. Keratin: protective top layer – dead cells
b. Dryness of skin is a major factor in inhibiting microbial growth on the skin
c. Periodic shedding of the epidermis helps remove microbes on the skin’s surface

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5
Q

The intact surface of healthy epidermis is rarely penetrated by microorganisms. When the epithelial surface is broken, which bacterial infection is most likely to occur?

A

Staphylococci infections:

Staph. normally inhabit the epidermis, hair follicles, sweat and oil glands of the skin

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6
Q

What is mucus? Where is it secreted?

A
  1. Mucus: a lightly viscous glycoprotein produced by goblet cells of a mucous membrane (epithelial layer)
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7
Q

Lacrimal apparatus

  1. What is it consisted of?
  2. How does it function in the defense system?
A
  1. A group of structures that manufactures and drains away tears – Lacrimal glands, upper eyelid, lacrimal canal, nasolacrimal duct, nose
  2. Tears are produced in the lacrimal glands, then passed under the upper eyelid. Tears then pass toward the corner of the eye near the nose and into lacrimal canals to the nose.
    a. The tears are spread over the surface of the eyeball by blinking. Normally, the tears evaporate or pass into the nose as fast as they are produced.
    b. This continual washing action helps keep microorganisms from settling on the surface of the eye.
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8
Q

Saliva: how does it function in the defense system?

A

Saliva is produced by the salivary glands.

a. Saliva helps dilute the numbers of microorg’s and wash them from both the surface of the teeth and the mucous membrane of the mouth.
b. This helps prevent colonization by microbes

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9
Q

Sebum

  1. What is sebum? and its composition
  2. pH
A

a. Sebum is produced by sebaceous glands; Sebum prevents hair from drying and becoming brittle.
b. Sebum also forms a protective film over the surface of the skin.
c. One of the components of sebum is unsaturated FAs, which inhibit the growth of certain pathogenic bacteria and fungi.
d. The low pH of the skin, b/w pH 3 and 5, is caused in part by the secretion of FAs and lactic acid.

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10
Q

Perspiration function in defense mech.

A
  1. Perspiration helps eliminate certain wastes and flush microorganisms off the skin
  2. Perspiration also contains lysozyme, which is capable of breaking down cell walls of Gram (+) bacteria and to a lesser extent, Gram (-) bacteria.
    a. Lysozyme breaks chemical bonds on peptidoglycan.
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11
Q

Microbial antagonism (3)

A

The normal microbiota prevent pathogens from colonizing the host

  1. By competing w/ them for nutrients (competitive exclusion)
  2. By producing substances that are harmful to the pathogens
  3. By altering conditions that affect the survival of the pathogens, such as pH and O2 availability
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12
Q

Leukocytosis

A
  1. Leukocytosis: an increase in total number of WBCs
  2. Leukopenia: a decrease in the leukocyte count
    a. Related to either impaired WBC production or the effect of increased sensitivity of WBC membranes to damage by complement, antimicrobial plasma proteins.
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13
Q

How are Phagocytes activated?

A
  1. Phagocytes may be activated by components of bacteria such as lipid A or LPS
  2. Small protein hormones secreted by phagocytes and other cells involved in immunity called cytokines
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14
Q

4 phases of phagocytosis

A
  1. Chemotaxis
  2. Adherence
  3. Ingestion
  4. Digestion
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15
Q

Opsonization

A

Microorganisms are first coated with serum proteins, which act as opsonins, and promote attachment of the microorganisms to the phagocyte

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16
Q

Dermis: what is it composed of?

A

Connective tissue

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17
Q

Epidermis: what is its main composition?

A

Many layers of continuous sheets of tightly packed epithelial cells, w/ little or no material b/w the cells.

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18
Q

What is the top layer of epidermal cell?

A

Dead cells, which contains a protective protein called keratin.

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19
Q

What is Leukocytosis?

A

The total # of WBCs increases as a protective response to combat the microbes.

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20
Q

What is Leukopenia?
What diseases can cause Leukopenia?
What causes the decrease?

A
  1. A decrease in leukocyte count.
  2. Ex: Salmonellosis, Brucellosis and some viral and rickettsial infections.
  3. May be related to either impaired WBC production or the effect of increased sensitivity of WBC membranes to damage by complement, antimicrobial plasma proteins.
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21
Q

Leukocytes are divided into two main categories, what are they? List the different type of cells in each category

A
  1. Granulocytes:
    Neutrophil, Basophil, Eosinophil
  2. Agranulocytes
    Monocyte, Lymphocyte
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22
Q

Color stains of the following cells:

  1. Neutrophils
  2. Basophils
  3. Eosinophils
A
  1. Neutrophils: pale lilac w/ acidic and basic dyes
  2. Basophils: blue-purple w/ basic dye methylene blue
  3. Eosinophils: red-orange w/ acidic dye eosin
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23
Q

In bacterial infection, which leukocyte(s) dominate(s) at the initial stage?
How about viral, fungal infections?

A
  1. Neutrophils dominate and then Macrophages dominate

2. In viral and fungal infections, Macrophages predominate in all phases of defense

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24
Q

What substance does Basophil release?

A

Histamine, which is important in inflammation and allergic responses

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25
Q

Which leukocyte releases histamine?

A

Basophil

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26
Q

What is Eosinophil’s role in destroying helminths?

A

Eosinophil can attach to the outer surface of the parasites and discharge peroxide ions that destroy helminths.

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27
Q

What are the two types of Macrophages? Where are they found?

A
  1. Fixed macrophage (aka. histiocytes)
    - - Found in liver (Kupffer’s cells), lungs (alveolar macrophages), nervous system (microglial cells), bronchial tubes, spleen, lymph nodes, red bone marrow and the peritoneal cavity surrounding the abdominal organs
  2. Wandering macrophage
    - - Roaming in the tissues and gathering at sites of infection or inflammation
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28
Q

What is the 4-step mechanism of phagocytosis?

A
  1. Chemotaxis
  2. Adherence – if microbes are coated with serum proteins that promote attachment of the microbes to the phagocyte, it’s called Opsonization
  3. Ingestion – pseudopods forming phagosome or phagocytic vesicle. The mem. of the phagosome has enzymes that pump protons into the phagosome, reducing the pH to ~4, at which hydrolytic enzymes are activated
  4. Digestion – Phagosomes and lysosomes fuse to form phagolysosome.
    - - Lysozymes hydrolyze peptidoglycan in bacterial cell walls.
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29
Q

What kinds of enzymes are in lysosomes?

A
  • Lysozyme
  • Proteases
  • Lipases
  • Ribonuclease
  • Deoxyribonuclease
  • Enzymes producing toxic O2 products (via oxidative burst) such as superoxide radical, hydrogen peroxide, singlet oxygen and hydroxyl radical
30
Q

Give examples of bacterial structures that inhibit adherence

A

M protein (ex. S. progenes) & capsules (ex. S. pneumoniae, H. influenzae type b)

31
Q

How does Leukocidin prevent phagocytosis?

A

Kill phagocytes by causing the release of the phagocyte’s own lysosomal enzymes into its cytoplasm.
- Ex. Staphylococcus

32
Q

How does Streptolysin prevent phagocytosis?

A

Similar to Leukocidin

33
Q

What are the 4 usual Signs and Symptoms for inflammation?

A

Redness
Pain
Heat
Swelling

34
Q

What are the functions of inflammation?

A
  1. To destroy the injurious agent
  2. To limit the effects on the body by confining or walling off the injurious agent and its by-products
  3. To repair or replace tissue damage by the injurious agent or its by-products
35
Q

What are the 3 stages of inflammation process?

A
  1. Vasodilation and increased permeability of blood vessels
  2. Phagocyte migration and phagocytosis
  3. Tissue repair
36
Q

Vasodilation stage of the inflammation process

A

Increase blood flow to the damaged area and is responsible for the redness (Erythema) and heat

37
Q

What are the possible causes of pain during inflammation?

A
  1. Nerve damage
  2. Irritation by toxins
  3. The pressure of edema
38
Q

What is the cause of edema during inflammation?

A

Vasodilation increases permeability, permitting fluid to move from the blood into tissue spaces, causing Edema

39
Q

What chemicals are responsible for vasodilation during inflammation?

A
  1. Histamine – Damaged cells cause release of histamine (present esp. in mast cells in connective tissue, circulating basophils and blood platelets)
  2. Kinins – present in blood plasma
  3. Prostaglandins – released by damaged cells, intensifying the effects of Histamine and Kinins and helping phagocytes move the. capillary walls
  4. Leukotrienes – produced by mast cells (mostly present in connective tissue of the skin and rest. sys, and in blood vessels) and basophils.
40
Q

What is Margination?

A

The sticking of phagocytes (both neutrophils and monocytes) to the inner surface of the endothelium of blood vessels.

41
Q

What is Emigration?

A

The collected phagocytes begin to squeeze b/w the endothelial cells of the blood vessel to reach the damaged area

42
Q

When does pus form?

A

After granulocytes or macrophages engulf large #s of microbes and damaged tissues, they themselves eventually die. As a result, pus forms.

43
Q

Tissue repair: how is tissue considered repaired?

A

A tissue is repaired when its stroma or parenchyma produces new cells
Stroma: the supporting connective tissue
Parenchyma: the functioning part of the tissue

44
Q

How does a perfect or near-perfect reconstruction of the tissue occur?

A
  1. If only parenchymal cells are active in repair, a perfect or near-perfect reconstruction of the tissue occurs
  2. If repair cells of the stroma of the skin are more active, scar tissue is formed.
45
Q

How does fever occur during inflammation?

A
  1. Body temp. is controlled by hypothalamus
  2. When phagocytes ingest Gram (-) bact, LPSs are released, causing the phagocytes to release IL-1, which causes hypo. to release prostaglandins that reset the hypo. thermostat. at a higher temp., thereby causing fever
  3. Another cytokine called alpha-TNF, produced by macrophages and mast cells, also induces fever
46
Q

What are the body changes to adjust to the new thermostat setting (fever)?
(3 changes)

A
  1. Blood vessel constriction
  2. Increased rate of metabolism
  3. Shivering (the body temp. is climbing higher than normal, but the skin remains cold, causing shivering)

The body will continue to maintain this new temp. until the IL-1 is eliminated

47
Q

Benefits of Fever: 3

A
  1. IL-1 helps set up production of T lymphocytes
  2. High temp intensifies the effect of interferons: inhibiting growth of some microbes by decreasing iron availability
  3. High temp. speeds up reactions in the body: accelerating tissue repair
48
Q

Complications of Fever: 7

A
  1. Tachycardia (rapid heart rate)
  2. increased metabolic rate, which may produce acidosis
  3. Dehydration
  4. Electrolyte imbalance
  5. Seizures in young children
  6. Delirium
  7. Coma
49
Q

At what body temp., death results?

A

44-46C (112-114F)

50
Q

List the components of the complement system

A

The complement sys. is a defensive sys. consisting of >30 proteins produced by the liver and could circulating in blood serum.
C3 (C3a, C3b), C5 (C5a, C5b), C6, C7, C8, C9

51
Q

What is MAC? How does it act in the complement system?

A

MAC: mem. attack complex
C5bC6C7C8C9
– Attaches to the microbe’s plasma membrane, making.a hole and cause water to enter the cell and ions to leave the cell.

52
Q

Is Gram (+) or Gram (-) bacteria more susceptible to MAC?

A

Gram (-): because there is only one or very few layers of peptidoglycan to protect the plasma membrane from the complement sys.

53
Q

Classical pathway of the Complement sys:

  1. How is C1 activated?
  2. How does C1 activate C2 and C4?
  3. How is C3 activated?
A
  1. ONE PAIR of antibody attaches to an antigen, forming the antigen-antibody complex –> Binds to C1 and activates it
  2. C1 splits C2 and C4 into a and b fragments
  3. C2a+C4b combine and TOGETHER activate C3 (split into C3a and C3b)

NOTE: C2a and C4b combine

54
Q

Alternative pathway of the Complement sys.:

How is C3 activated?

A

Factor B, D, P on the surface of the pathogen bind to C3, which activates C3 by splitting it into a and b fragments

55
Q

Lectin pathway of the Complement sys:

Describe the process how C3 is activated in 4 steps

A
  1. After Macrophage phagocytosis, some chemicals are released to stimulate the liver to produce LECTIN (aka. mannose binding lectin – MBL)
  2. Lectin binds to Mannose present in the microbial cell walls (bacteria and some viruses)
  3. TOGETHER (Lectin+mannose) acts as an opsonin, enhancing phagocytosis and activates C2 and C4
  4. C2 and C4 are activated by splitting into a and b fragments, C2a+C4b combine and activates C3
56
Q

How do some microbes evade the Complement Sys?

List 3 ways

A

By means of

  1. Capsules: Sialic acid- discourages opsonization and MAC formation
  2. Surface lipid-carb. complexes: Some Gram (-) bact. – lengthen surface lipid-carb complexes to prevent MAC formation
  3. Enzymatic destruction of C5b: Gram (+) cocci – release an enzyme that breaks down C5a (a chemotactic factor that attracts phagocytes)
57
Q

What are the 3 types of Interferons? Where are they produced?

A
  1. Alpha-IFN
    Beta-IFN
    Gamma-IFN (produced by lymphocytes)
  2. They are produced by fibroblasts in connective tissue, by lymphocytes and other leukocytes
58
Q

Function of alpha and beta-IFN

A
  1. alpha and beta IFN are produced by viral infected cells in small quantities, which then diffuse to uninfected neighboring cells
  2. They react w/ plasma or nuclear mem. receptors, inducing the UNINFECTED cells to manufacture mRNA for the syn. of Antiviral Proteins
59
Q

Function of gamma-IFN

A
  1. Gamma-IFN is produced by lymphocytes, which induce Neutrophils and Macrophages to kill BACTERIA by phagocytosis
  2. Injection of IFN can work as antiviral
60
Q

Clinical use of IFN and the side-effects

A
  1. CGD (chronic granulomatous disease): neutrophils and macrophages do not kill bacteria
    - - Take recombinant gamma-IFN for lifetime
  2. Side effects: nausea, fatigue, headaches, vomiting, weight loss and fever
  3. High conc. of IFN is toxic to the heart, liver, kidneys and red bone marrow.
61
Q

Give two examples of AVPs and their functions

A
  1. Oligoadenylate synthetase: degrades viral mRNA

2. Protein kinase: inhibits protein synthesis

62
Q

Which of the following does not stimulate phagocytes?

a. Cytokines
b. gamma-IFN
c. C3b
d. Lipid A
e. Histamine

A

E

63
Q

Legionella uses C3b receptors to enter monocytes. This

a. prevents phagocytosis
b. degredes complement
c. Inactivates complement
d. Prevents inflammation
e. prevents cytolysis

A

C?

64
Q

Chlamydia can prevent the formation of phagolysosomes, and therefore Chlamydia can

a. avoid being phagocytized
b. avoid destruction ion by complement
c. prevent adherence
d. avoid being digested
e. none of the above

A

D

65
Q
The skin and mucous mem. are the body's first line of defense against pathogens. This function results from both mechanical and chemical factors. 
List the Mechanical factors
1. Skin
2. Mucous
3. Lacrimal apparatus
4. Saliva
5. Urine and vaginal secretions
A
  1. The structure of intact skin and the waterproof protein keratin provide resistance to microbial invasion
  2. Mucus traps many microbe that enter the respiratory and GI tracts; in the lower respiratory tract, the ciliary escalator moves mucus up and out
  3. The lacrimal apparatus protects the eyes from irritating substances and microorganisms
  4. Saliva washes microbe from teeth and gums
  5. The flow of urine moves microbe out of the urinary tract, and vaginal secretions move microbes out of the vagina
66
Q

Transferrin in the blood: function in defense mech

A

Transferrin: iron-binding protein
– Inhibit bacterial growth by reducing the amt. of available iron, which is not only required for microbial growth (syn. of cytochromes and enzymes), it also suppress chemotaxis and phagocytosis

Iron overload increases the risk of infection

67
Q

If the following are placed in the order of occurrence, which would be the third step?

a. Emigration
b. Digestion
c. Formation of a phagosome
d. Formation of a phagolysosome
e. Margination

A

C

68
Q

If the following are placed in the order of occurrence, which would be the third step?

a. Activation of C5-C9
b. Cell lysis
c. Antigen-antibody rxn
d. Activation of C3
e. Activation of C2-C4

A

D?

69
Q

Which of the following stmts about alpha-IFN is not true?

a. It interferes w/ viral replication
b. It is host specific
c. It is released by fibroblasts
d. It is virus-specific
e. It is released by lymphocytes

A

C

70
Q

A decrease in the production of C3 would result in

a. increased susceptibility to infection
b. increased numbers of WBCs
c. increased phagocytosis
d. activation of C5-C9
e. none of the above

A

A?

71
Q

In 1884, Elie Metchnikoff observed blood cells collected around a splinter inserted in a sea star embryo. This was the discovery of

a. blood cells
b. sea stars
c. phagocytosis
d. immunity
e. none of the above

A

E?