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Clinical Microbiology > (exam 2) ch 16 Innate immunity: Nonspecific defenses of the host > Flashcards

(exam 2) ch 16 Innate immunity: Nonspecific defenses of the host Flashcards

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Biology 101 flashcards
1
Q

what is susceptibility?

A

lack of resistance to a disease

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2
Q

what is immunity?

A

ability to ward off disease

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3
Q

what does the body’s first line of defense consist of?

A

skin, mucous membranes, and antimicrobial substances

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4
Q

what does the body’s second line of defense consist of?

A

inflammation, fever, and phagocytes

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5
Q

what does the body’s third line of dense consist of?

A

humoral and cellular response

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6
Q

which lines of defense by the body is innate immunity?

A

first and second lines of defense

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7
Q

which lines of defense by the body is adaptive immunity?

A

third line of defense

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8
Q

what is innate immunity?

A

defenses against any pathogen (broad scope); rapid and present at birth

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9
Q

what is adaptive immunity?

A

immunity or resistance to a specific pathogen; slower to respond, has memory component

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10
Q

Toll-like receptors (TLRs) on host defense cells, attach to what structure of pathogens?

A

attach to pathogen-associated molecular patterns (PAMPs)

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11
Q

what are pathogen-associated molecular patterns (PAMPs) ?

A

PAMPs are molecular structures common to pathogens

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12
Q

what are some examples of structures on pathogens that host cells recognize as foreign?

A

host cells recognize the following as foreign because it is stuff the host cells do not have:

1) LPS outer membrane of gram negative bacteria
2) Peptidoglycan cell wall in gram positive bacteria
3) flagellin (protein) in flagella
4) DNA and RNA of viruses

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13
Q

when the TLRs (of host cells) bind to the PAMPs (of the pathogens) what response does this induce from the host cells?

A

induces the release of cytokines from the host defensive cells (innate system)

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14
Q

what are cytokines?

A

small cell signaling proteins that regulate the intensity and duration of the hosts immune responses link between innate and adaptive immunity

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15
Q

how does the initial release of cytokines signal the innate immune system and the adaptive immune system?

A

1) innate - recruits defensive cells to isolate and destroy microbes as part of inflammatory response
2) adaptive- can activate cells involved in adaptive immunity

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16
Q

what two portions make up the skin (first line defense) ?

A

epidermis and dermis

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17
Q

what is the epidermis?

A

outer portion of the skin made of tightly packed epithelial cells containing keratin, a protective protein

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18
Q

what is the dermis?

A

inner portion made of connective tissue

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19
Q

how does the keratin in the epidermis inhibit microbial growth?

A

Shedding and dryness of skin inhibits microbial growth

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20
Q

what are the mucous membranes (first line of defense)?

A

Epithelial layer that lines the gastrointestinal, respiratory, and genitourinary tracts

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21
Q

what two structures of mucous membranes are important to stopping entry of microbes?

A

mucus and cilia

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22
Q

what is mucus? how is this important to stopping microbes?

A

viscous glycoproteins that trap microbes and prevent tracts from drying out

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23
Q

what is cilia? how is this important to stopping microbes?

A

little hairs; Ciliary escalator transports microbes trapped in mucus away from the lungs; propels them upwards towards the throat

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24
Q

what is the Lacrimal apparatus?

A

in the eye; it drains tears and washes eye

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25
Q

what are are some chemical factors of the first line defense?

A

many secretions of the skin and mucous membranes lower the pH environment to inhibit or destroy microbes (bc most microbes grow at a pH of 7)

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26
Q

what chemical factor of sebum helps inhibit / destroy microbes?

A

sebum forms a protective film and lowers the pH of the skin to around 3-5

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27
Q

what is in tears, saliva and urine that helps to destroy microbes and how does it target them?

A

lysosome in these perspirations destroys bacterial cell walls which helps kill microbes

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28
Q

how does the normal microbiota help inhibit microbial growth?

A

normal microbiota compete with pathogens via microbial antagonism (competitive exclusion)

  • compete for space and nutrients
  • produce substances harmful to pathogens
  • alter conditions to affect pathogen survival
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29
Q

what are probiotics and how do they effect microbial growth?

A

probiotics live microbial cultures administered to exert a beneficial effect; Often lactic acid bacteria which produce lactic acid and bacteriocins that inhibit pathogen growth

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30
Q

what portions are two components in the blood?

A

1) plasma (fluid portion)

2) formed elements

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31
Q

what are the formed elements of the blood?

A

1) Erythrocytes (red blood cells)
2) Leukocytes (white blood cells)
3) Platelets

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32
Q

where are the formed elements of the blood made?

A

created in red bone marrow stem cells

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33
Q

how are the formed elements of the blood made?

A

made via hematopoiesis

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34
Q

what is hematopoiesis ?

A

Creation of blood cellular components

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35
Q

all blood cells arise from what type of cells?

A

pluripotent stem cells

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36
Q

Leukocytes are important for what type of immunity?

A

innate immunity

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37
Q

there are two types of leukocytes and these are divided into two types by what?

A

by appearance under light microscope

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38
Q

what are the two main types of leukocytes?

A

granulocytes and agranulocytes

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39
Q

what are granulocytes?

A

visible granules in cytoplasm

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40
Q

what are agranulocytes?

A

granules in cytoplasm that are not visible via light microscopy

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41
Q

what are three types of granulocytes?

A

1) neutrophils
2) basophils
3) eosinophils

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42
Q

what are neutrophils?

A

(type of granulocytes) phagocytic; work in early stages of infection; can leave the blood and enter infected tissue; type of polymorphonuclear cells (PMNs)

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43
Q

what are basophils?

A

(type of granulocytes) release histamine; mediate inflammation and allergic responses; type of polymorphonuclear cells (PMNs)

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44
Q

what are eosinophils?

A

(type of granulocytes) phagocytic; toxic against parasites and helminths; can leave the blood; type of polymorphonuclear cells (PMNs)

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45
Q

what are three types of agranulocytes?

A

1) monocytes
2) dendritic cells
3) lymphocytes

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46
Q

what are monocytes?

A

(type of agranulocytes) leave blood, enter body tissues, and mature into macrophages (become phagocytic)

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47
Q

what are dendritic cells?

A

(type of agranulocytes) found in the skin, mucous membranes, and thymus; phagocytic, initiate adaptive responses

48
Q

what are lymphocytes?

A

(type of agranulocytes) T cells, B cells, and NK cells; play a role in adaptive immunity

49
Q

what are differential while blood cell counts?

A

a measure of leukocytes in the blood; % per 100 cells counted

50
Q

what can high white blood cell counts indicate?

A

may indicate bacterial infections, autoimmune diseases or side effects of medications

51
Q

what is the term for high white blood cell counts?

A

leukocytosis

52
Q

what can low white blood cell counts indicate?

A

may indicate viral infections, pneumonia, autoimmune diseases or cancer

53
Q

what is the term for low white blood cell counts?

A

leukopenia

54
Q

what is lymph?

A

fluid

55
Q

what are lymphatic vessels?

A

vessels, similar to the circulatory system

56
Q

what are lymphatic tissues?

A

scattered throughout mucous membranes that line GI, respiratory, urinary, and reproductive organs

57
Q

what are four specific organs and aggregations of lymphoid tissues?

A

1) spleen
2) thymus
3) tonsils
4) Peyer’s patches

58
Q

what is phagocytosis?

A

the ingestion of microbes or other substances by a cell; performed by phagocytes

59
Q

what are the four steps to the mechanism of phagocytosis?

A

1) chemotaxis
2) adherence
3) ingestion
4) digestion

60
Q

what is chemotaxis?

A

first step in phagocytosis; chemical signals attract phagocytes to microorganisms

61
Q

what is adherence?

A

second step in phagocytosis; attachment of a phagocyte to the surface of the microorganism (TLRs and PAMPs) and is enchanted by opsonization

62
Q

what is opsonization?

A

process that marks microbial antigens with serum proteins (marks them for destruction) (can be done by antibodies)

63
Q

what is ingestion?

A

third step in phagocytosis; pseudopods (plasma membrane extensions) engulf microbe; pseudopods meet, fuse, and form a phagosome (internal pH shifts to 4); phagosome pinches off membrane and enters cytoplasm

64
Q

what is digestion?

A

four step in phagocytosis; phagosome contacts and fuses with lysosome (contains digestive enzymes and bactericidal substances) forming a phagolysosome which then digests the microorganism. Phagolysosome (now called “residual body” releases indigestible material outside the cell

65
Q

what is a phagosome?

A

a vacuole in the cytoplasm of a cell, containing a phagocytosed particle enclosed within a part of the cell membrane

66
Q

what is a phagolysosome?

A

cytoplasmic body formed by the fusion of a phagosome with a lysosome; its formation is essential for the intracellular destruction of microorganisms and pathogens

67
Q

how do you remember the signs and symptoms of inflammation?

A

“PRISH”

68
Q

what is inflammation?

A

local defense response triggered by injury to body tissue

69
Q

what are the signs and symptoms of inflammation?

A

1) Pain - release of chemicals
2) Redness - increased blood flow
3) Immobility - loss of function in severe cases
4) Swelling - fluid accumulation
5) Heat - increased blood flow

70
Q

what are three functions of inflammation?

A

1) Destroys injurious agent; removes it and by-products
2) Limits its effects on the body; isolating / walling off it and by-products
3) Repairs and replaces damaged tissue; by the injurious agent and buy products

71
Q

what are two types of inflammation?

A

acute or chronic inflammation

72
Q

what is acute inflammation?

A

Primarily caused by neutrophils; rapid development of signs and symptoms, last days to weeks; mild and self-limiting (appendicitis, cold, flu, sore throat, minor cuts/scratches)

73
Q

what is chronic inflammation?

A

Primarily caused by monocytes and macrophages; slow development of signs and symptoms; last months to years; more severe and progressive (mononucleosis, peptic ulcers, tuberculosis, rheumatoid arthritis)

74
Q

macrophage TLRs recognize PAMPs and release cytokines (TNF-alpha) — the liver responds to TNF-alpha in the blood and activates what? what does this do?

A

activates acute-phase proteins; serum concentration changes (+/-) by >25% in response to cytokines; indication of inflammation

75
Q

what are the three STEPS in the inflammation process in the body?

A

1) Vasodilation and increased permeability of blood vessels
2) Phagocyte migration and phagocytosis
3) Tissue repair

76
Q

what happens during Vasodilation and increased permeability of blood vessels ?

A

Both of these occur immediately following tissue damage; vasodilation = dilation of blood vessels; increased permeability = defensive substances can leave blood vessels and enter injured area

77
Q

what does vasodilation cause?

A

causes redness (erythema) and heat

78
Q

what does increased permeability cause?

A

causes fluid accumulation (edema)

79
Q

what causes vasodilation and increased permeability?

A

vasoactive mediators which are chemicals released by damaged cells that elicit a response

80
Q

what is the result of Vasodilation and increased permeability of blood vessels ?

A

an abscess forms = cavity created by breakdown of tissue containing pus (mixture of dead cells and body fluids)

81
Q

what is margination?

A

as blood flow decreases, phagocytes (neutrophils and monocytes) stick to the inner surface of blood vessel (caused by cytokines)

82
Q

what is diapedesis?

A

(after margination occurs) phagocytes squeeze between endothelial cells of blood vessels

83
Q

when can tissue be repaired?

A

when stroma or parenchyma produce new cells

84
Q

what is parenchyma and how is the tissue repair?

A

functioning part of the tissue that is repaired; near perfect repair

85
Q

what is the stroma and how is the tissue repair?

A

supporting connective tissue that is repaired; scar tissue

86
Q

how does scar tissue arise?

A

(with chronic inflammation) cytokines released by macrophages cause stroll cells to synthesize connective tissue (fibrosis)

87
Q

what is fibrosis?

A

accumulation of connective tissue resulting in scar tissue

88
Q

what is fever?

A

abnormally high body temperature; overall systemic response to infection

89
Q

what typically causes fever?

A

typically caused by bacterial or viral infection; released cytokines cause the hypothalamus to reset to higher temperature; higher temperature is maintained until cytokines are eliminated

90
Q

is fever a good defense against disease?

A

to a certain point; it increases production and effects of certain antimicrobial molecules but complications can be worse; these include dehydration, rapid heart rate, electrolyte imbalances (death above 44-46 decreases celsius)

91
Q

what is the complement system?

A

> 30 proteins produced by the liver that circulate and blood serum and body tissues; aids and enhancing immune system ability to destroy microbes

92
Q

how are complement proteins labeled?

A

Designated with uppercase C and numbered in order of discovery
(inactive until split into fragments)
Activated fragments indicated with lowercase a and b (i.e C3a)

93
Q

what do we know about complement activation?

A

proteins act in a cascade, one reaction triggers another?

94
Q

what are the three activation pathways resulting in activation of C3?

A

1) classical
2) alternative
3) lectin

95
Q

what is the classical pathway resulting in activation of C3?

A

initiated when antibodies bind antigens; results in C3a and C3b (activated)

96
Q

what is the alternative pathway resulting in activation of C3?

A

activated by contact between complement proteins and microbe; results in C3a and C3b (activated)

97
Q

what is the lectin pathway resulting in activation of C3?

A

initiated when lectins bind carbohydrates on microbe surface; results in C3a and C3b (activated)

98
Q

what are three outcomes of the complement activation?

A

1) cytolysis
2) opsonization
3) inflammation

99
Q

what is cytolysis, one of the outcomes of complement activation?

A

activated complement proteins create a membrane attack complex (MAC); this creates hole in plasma membrane and fluid inflow bursts the cell-lysis

100
Q

cytolysis is more effective against what type of bacteria and why?

A

more effective against Gram negative bacteria due to their thinner peptidoglycan wall

101
Q

what is opsonization, one of the outcomes of complement activation?

A

activated complement proteins promotes attachment of phagocytes to microbe

102
Q

what is inflammation, one of the outcomes of complement activation?

A

activated complement proteins bind to mast cells, releasing histamine which increases inflammation

103
Q

how is the complement system regulated?

A

regulatory proteins readily break down complement proteins, minimizing host cell destruction

104
Q

what can happen if a person has a lack of complement proteins?

A

they can be more susceptible to infections

105
Q

what is one structure that allows microbes are able to evade the complement system?

A

CAPSULES prevent complement activation

106
Q

what are interferons (IFNs)?

A

class of cytokines with antibacterial and antiviral activity; great variation between types

107
Q

what are three primary types of human IFNs?

A

1) IFN-a (alpha)
2) IFN-b (beta)
3) IFN-y (gamma)

108
Q

what are IFN-a and IFN-b?

A

produced by cells in response to viral infections; cause neighboring cells to produce antiviral proteins (AVPs) that inhibit viral replication (prevents spreads of viral infection to non-infected cells-stopping infection)

109
Q

what are IFN-y?

A

causes neutrophils and macrophages to kill bacteria

110
Q

what are iron-binding proteins?

A

iron is essential for survival of humans and pathogens; concentration of free iron in the body is low due to competition between human cells and pathogens for iron

111
Q

what is transferrin?

A

(human iron binding proteins) found in blood and tissue fluids

112
Q

what is lactoferrin?

A

(human iron binding proteins) found in milk, saliva, and mucus

113
Q

what is ferritin?

A

(human iron binding proteins) found in the liver, spleen, and red bone marrow

114
Q

what is hemoglobin?

A

(human iron binding proteins) located in red blood cells

115
Q

bacteria produce _____________ which pull iron form host to compete with iron-binding proteins of the host

A

siderophores

116
Q

what are antimicrobial peptides?

A

short peptides produced in response to protein and sugar molecules on microbes

Clinical Microbiology (17 decks)

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