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Microbio > 260 Final > Flashcards

260 Final Flashcards

1
Q

i. Are well established microbes that don’t cause an overt disease but provide a protective shield against pathogens

A

normal body flora

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2
Q
  1. Receive nutrients from the host

2. Locate themselves depending upon their food source

A

Resident flora

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3
Q

Locate themselves depending upon their food source

a. Fatty acids
b. Mucus – proteins & carbs
c. Secretions and digested food of the digestive tract

A

Resident flora

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4
Q

i. Produced by skin’s sebaceous glands

ii. Even sweat includes nutrient molecules

A

fatty acids

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5
Q

i. Linings of
1. Respiratory
2. Digestive
3. Reproductive tract

A

Mucus - proteins and carbs

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6
Q

i. Saliva contains mucin (active ingredient in mucus) and food particles

A

c. Secretions and digested food of the digestive tract

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7
Q

ii. Few organisms survive the acids in the stomach and enzymes of the small intestines

A

c. Secretions and digested food of the digestive tract

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8
Q

iii. Large intestine supports 10 trillion microbes including Archaea

A

c. Secretions and digested food of the digestive tract

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9
Q
  1. Normal flora receive nutrients from host and are essential to the health of humans
A

iii. Maintenance of the Normal Resident Flora

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10
Q
  1. Flora create an environment that may prevent infections and can enhance host defenses
A

iii. Maintenance of the Normal Resident Flora

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11
Q
  1. Antibiotics, dietary changes, and disease may alter flora
A

iii. Maintenance of the Normal Resident Flora

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12
Q
  1. Associated with areas in direct contact with the environment
  2. Inhabit the body sporadically and do not acquire nutrients
A

iv. Transient flora

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13
Q
  1. Positive and obligatory relationship for both organisms
A

Mutualism

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14
Q
  1. Ex: eukaryotic cells and their mitochondria, infants, and vitamin A producing bacteria
A

Mutualism

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15
Q
  1. Is a positive relationship for both organisms but non-obligatory (normal body flora)
A

Synergism

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16
Q
  1. Humans and the bacteria in our digestive tracts
A

Synergism

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17
Q

a. Bacteria synthesize growth factors
i. Vitamins B12
ii. K
iii. Niacin
iv. Thiamin
v. Riboflavin
vi. Folic acid

A

Synergism

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18
Q

b. Assists with the breakdown of fibrous wastes

c. Stimulate development of the immune system

A

Synergism

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19
Q
  1. When a relationships is positive for one organism, and neutral for the other organism (normal body flora)
A

Commensalism

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20
Q
  1. Microbes on our skin that consume skin secretions
A

Commensalism

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21
Q
  1. Lactic acid bacteria that lower pH of female reproductive tract
A

Commensalism

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22
Q
  1. When one organism benefits and the other is harmed (disease)
A

Parsitism

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23
Q
  1. When both organisms are harmed

2. Disease

A

Competition

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24
Q
  1. When microbes are present
A

Contamination

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25
Q
  1. When microbes exist superficially as reproducing surface populations
A

Colonization

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26
Q
  1. When microbes enter the tissue
A

Infection

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27
Q
  1. When there is noticeable impairment of body function
A

Disease

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28
Q

i. Involves a microbe vs. noninfectious

A

Infectious

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29
Q

i. When an infectious disease can spread from one person to another person

A

Communicable

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30
Q

i. When a communicable disease is easily spread from host to host

A

Contagious

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31
Q

i. Caused by microbes from outside of the body

A

Exogenous

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32
Q

i. Caused by microbes already present in or on the body

A

Endogenous

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33
Q

i. When a microbe can cause a disease only in hosts with impaired immune systems or when relationships become unbalanced.

A

Opportunistic

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34
Q

i. Characteristics of a disease that can only be felt or observed by the patient

A

Symptoms

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35
Q
  1. Headache
  2. Cramps
  3. Nausea
  4. Pain
  5. Irritatio
  6. Malaise
  7. Fatigue
  8. Chest tightness
  9. Itching
  10. Headache
  11. Weakness
  12. Anorexia
  13. Sore throat
A

Symptoms

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36
Q

i. Characteristics of a disease that can be observed by examining the patients

A

Signs

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37
Q
  1. Changes in leukocyte count
  2. Inflammation and fever
  3. Elevated antibody titer in the blood
  4. Septicemia
  5. Microbes in tissue fluids
  6. Abnormal chest sounds
  7. Skin eruptions
  8. Swollen lymph nodes
  9. Absecesses
  10. Tachycardia (increased heart rate)
  11. Changes in urinr constituents
A

Signs

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38
Q

i. Over 10,000 white blood cells/uL

A

Leukocytosis

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39
Q

i. Under 10,000 WBC’s/uL

A

Leukopenia

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40
Q

i. Combination of signs and symptoms

A

Syndrome

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41
Q

d. Headache

A

i. Neutral microbe

ii. Negative to host

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42
Q

e. Fever

A

i. Negative microbe

ii. Positive to host

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43
Q

f. Inflammation

A

i. Negative microbe

ii. Positive to host

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44
Q

g. Cramps -> diarrhea

A

i. Positive microbe

ii. Positive host

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45
Q

h. Nausea –> vomiting

A

i. Positive microbe

ii. Positive host

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46
Q

i. Coughing

A

i. Positive microbe

ii. Positive host

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47
Q

j. Sneezing

A

i. Positive microbe

ii. Positive host

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48
Q

k. Runny nose

A

i. Positive microbe

ii. Positive host

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49
Q

nonspecific barriers to microbial entry with which a person is born; present at birth; no memory

A

a. Innate Immunity

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50
Q
  1. Prevents infection
  2. Competitive Exclusion
  3. Physical Barriers
  4. Chemical barriers
A

First line of defense

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51
Q

a. When normal flora compete with invading microbes

A
  1. Competitive Exclusion
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52
Q

a. Skin
b. Mucous membranes
c. Flushing mechanisms
i. Coughing
ii. Sneezing
iii. Urination
iv. Tears
v. Cilia
vi. Peristalsis

A

Physical barriers 1st line

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53
Q

a. Acids in
i. Stomach
ii. Female reproductive tract (vagina)
b. Lysozyme found in
i. Tears
ii. Saliva
iii. Digests bacterial cell walls

A

Chemical barriers 1st line

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54
Q
  1. Prevents disease
  2. Chemicals
  3. Biological barriers
A

2nd line of defense

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55
Q

a. Complement

b. Interferon

A

Chemical barriers

2nd line of defense

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56
Q

i. Group of 20 blood proteins
ii. Bind to microbe membranes –> chain reaction leading to the insertion of pores in membranes of microbes (microbe lysis)

A

Complement

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57
Q

i. Antiviral
ii. Is produced by fibroblast and WBC’s invaded by a virus
iii. Attaches to receptor sites on neighboring host cells
iv. Activates an enzyme which blocks the translation of viral m-RNA and an enzyme that degrades viral m-RNA

A

Interferon

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58
Q
  1. In response to
    a. Virsues
    b. RNA
    c. Immune products
    d. Various antigens
A

Interferon

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59
Q
  1. Alpha
    a. Lymphocytes and macrophages
  2. Beta
    a. Fibroblasts & epithelial cells
  3. Gamma
    a. T cells
A

Interferon

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60
Q
  1. Induce expression of

a. Antiviral proteins

A

Interferon

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61
Q
  1. Inhibit expression of

a. Cancer genes

A

Interferon

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62
Q

iv. Activates an enzyme which blocks the translation of viral m-RNA and an enzyme that degrades viral m-RNA

A

Interferon

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63
Q

a. Phagocytosis
The absence of receptor sites on cell membranes
b. Inflammation

A

Biological barriers

2nd line of defense

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64
Q
  1. Via nonspecific leukocytes (=general WBC)
A

phagocytosis

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65
Q
  1. The most common WBC
  2. Effectively kill bacteria and other microbes
  3. General purpose
  4. React early to bacteria and other foreign materials, and to damaged tissues
  5. Lysozyme and defensins
A

Neutrophils

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66
Q
  1. The largest blood borne phagocytes
  2. Circulate for about 3 days in the blood;
  3. Then migrate into the tissues and become macrophages and dendritic cells
A

Monocytes

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67
Q
  1. Digest antigens into smaller antigenic determinants and present them to cells of the immune system
    - APC
A

Macrophages

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68
Q

anything foreign to the body that initiates an immune response

A

antigens

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69
Q

distinctive amino acid sequences that mobilizes the immune response

ii. AKA “exogenous” antigens
iii. AKA “epitopes”

A

antigenic determinants

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70
Q
  1. Bind to naïve TCD4 cells and secrete the lymphokine interleukin-1
A

macrophages

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71
Q

chemicals produced by WBCs that target other WBCs and influence their behavior

A

=lymphokine

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72
Q

i. Helps activate naïve TCD4 clls

A

Interleukin-1

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73
Q

ii. Stimulates the brain (hypothalamus) to raise the body’s temperature, FEVER, which
1) helps activate naïve TCD4 cells;
2) enhances the activity of immune cells (T cell production increases 20 fold if temperature up to 102.2) and interferon;
3) increases microbial demand for iron;
4) reduces host’s absorption of iron

A

Interleukin-1

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74
Q

iii. Inflammatory agent

iv. Also induces sleeps, aches, and pains

A

Interleukin-1

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75
Q
  1. Will phagocytize antigen and present (epitope) to immune cells
A

Macrophages

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76
Q
  1. APC
  2. Digests antigens into epitopes (antigenic determinants)
  3. Present epitopes to and activate both naïve TCD4 and naïve TCD8 cells
A

Dendritic cells

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77
Q

i. When tissues are injured, WBC’s (basophils and mast cells) release chemicals such as histamines, kinins, and prostaglandins

A

Inflammation

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78
Q

ii. Includes dilation, increased permeability of blood vessels

A

Inflammation

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79
Q
  1. “leaky capillaries”
  2. Redness, swelling, pain (edema), increased temperature, delivers immune component
  3. Localizes microbes and chemicals used for tissue repair.
A

Inflammation

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80
Q
  1. Adaptive
  2. The recognition and elimination of foreign and/or dangerous antigens
  3. Takes time to respond
  4. Has memory
  5. Prevents death
A

Acquired Immunity

Third Line of Defense

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81
Q

i. Are unique to each individual
ii. Identify self
iii. Are associated with the cell membrane of all nucleated cells of the body
1. NOT red blood cells

A

MHC-1

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82
Q

iv. Part of intracellular surveillance system, whereby enzymes regularly break down cytoplasmic proteins into peptides (epitopes) and transport the epitopes to the cell surface attached to said receptors

A

MHC-1

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83
Q

v. Its epitope complexes are examined by effector T killer/cytotoxic cells.
vi. Normal “self” epitopes are ignored while epitopes from an antigen that has infected the cell (or a cancer cell) will instigate an attack by the T-cellls

A

MHC-1

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84
Q

vii. Help to identify self (all nucleated cells)
viii. Intracellular surveillance (cell infected or cancerous)
ix. Monitored by T cytotoxic cells

A

MHC-1

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85
Q

i. Associated with the cell membrane of macrophages, B Lymphocytes and dendritic cells

A

MHC-II

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86
Q

ii. Part of the extracellular surveillance system

A

MHC-II

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87
Q

iii. When enzymes break down phagocytized antigens into epitopes, the peptides are transported to the cell surfaced attached to these receptors

A

MHC-II

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88
Q

i. Dendritic cells and macrophages present these complexes to naïve TCD4 cells while naïve B lymphocytes present its epitope complex to effector T helper cells

A

MHC-II

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89
Q

v. Only on macrophages, dendritic cells, and B lymphocytes (APC’s)
vi. Used for extracellular surveillance (cell phagocytized something)

A

MHC-II

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90
Q

vii. Used for TCD4 cells

A

MHC-II

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91
Q

a. In the bone marrow, lymphocytic stem cells differentiate into either

A

T or B cells

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92
Q

B cells stay in

T cells migrate

A

the bone marrow

to the thymus

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93
Q
  1. Get a T cell receptor

2. Allow T cell to recognize 1 specific antigen held in an MHC receptor

A

T cells in thymus

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94
Q
  1. Have to be able to identify “self”

4. Get a CD4 or CD8 receptor which allows them to attach to either MHC1 or MHC2 receptor

A

T cells in thymus

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95
Q
  1. Get a CD28 costimulatory receptor
A

T cells in thymus

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96
Q

b. Both then migrate to

A

secondary lymphoid tissue

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97
Q

a. Derived from bone marrow lymphoid stem cells that differentiate into immature lymphocytes with T cell receptors

A

T cells

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98
Q

recognition receptor that is complementary to and allows a T cell to identify an epitope from a specific microbe

A

T cell receptors

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99
Q

i. T cells whose T cell receptor an recognize “self” epitopes without binding too tightly survive their stay in the thymus

A

= positive selection

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100
Q

ii. T cells that bind inappropriately to self-epitopes are eliminated

A

negative selection

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101
Q
  1. Immature T cell acquires a CD8 receptor if thymic cells present self epitopes to the T cell via an
A

MHC 1 receptor

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102
Q
  1. Immature T cell acquires a CD4 receptor if thymic cells present self epitopes to the T cell via
A

MHC II

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103
Q

receptors are attachment receptors that help T cells bind to MHC-epitope complexes

A

CD4 and CD8

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104
Q

iii. Immature cells also acquire

A

CD28 recptor

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105
Q

i. Naïve TCD8 cells emerge from the thymus, each distinguished from the others by its unique

A

T cell receptor

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106
Q

iii. Dendritic cells have phagocytized and processed antigens into epitopes travel to lymph tissue and present those epitopes to naïve TCD8 cells in

A

MHC1

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107
Q
  1. If complementary, the T cell receptor binds to the
A

epitope

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108
Q

while

2. The CD8 receptor binds to

A

MCH 1 receptor

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109
Q

If dendritic cell’s ___ receptor have been activated (bound to antigens recognized as dangerous, e.g. flagellin), the dendritic cells will display co-stimulatory molecule ___ which bind to CD28 receptors on the TCD8 cell

A

toll-like

B7

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110
Q

increase in size, multiply, and differentiate into clones of specific effector T Killer/cytotoxic cells, and delayed hypersensitivity cells (involved in allergic reactions)

A

Activated T cells

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111
Q

a. Leaves lymphoid tissue and search for cells presenting MHC 1 epitop complexes with foreign epitopes complementary to their T cell receptor

A

Effector T cytotoxic cells

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112
Q

b. Synapse with MHC-I receptors presenting the foreign epitope

A

Effector T cytotoxic cells

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113
Q

c. Release lymphotoxins (like perforin) which form pores in the cell membrane of the infected cell and protreases which enter the infected cell through the pores and cuase the infected cell to undergo
apoptosis=programmed cell death

A

Effector T cytotoxic cells

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114
Q

also produce lymphokines that attract other lymphocytes and macrophages

A

Effector T cytotoxic cells

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115
Q

a. Involved in delayed hypersensitivity (allergic) reaction that may take several days to develop

A
  1. Delayed hypersensitivity cells
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116
Q

a. Result of affinity maturation where the cytotoxic cells with the best binding T cell receptors survive to reproduce and generate the “best” progeny

A

Memory T Cytotoxic Cells

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117
Q

b. Are long lived cells that remain in circulation after an adaptive immune response is over

A

Memory T Cytotoxic Cells

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118
Q

c. Ready to quickly become effector T cytotoxic cells

A

Memory T Cytotoxic Cells

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119
Q

d. Provide the basis for the quick anamnestic or secondary immune response, that occurs when the same antigen is encountered again (the basis of immunization programs)

A

Memory T Cytotoxic Cells

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120
Q

are most common of cells associated with adaptive immunity

A

TCD4

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121
Q

cells also emerge from the thymus, each distinguished from the other by its unique T cell receptor

A

TCD4

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122
Q

iii. Dendritic cells and macrophages that have phagocytized and processed antigens into epitopes present those epitopes to naïve TCD4 cells in

A

MHC II epitope complexes

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123
Q
  1. If complementary, T cell receptor binds to the epitope while
  2. The CD4 receptor binds to the
A

MHCII

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124
Q

If ___ have been activated on dendritic cell and/or macrophage, the presenting cells will display co-stimlatory molecules such as
___ which bind to receptors on the ___ cell

A

toll like receptors
b7 receptors
tcd4 cell

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125
Q
  1. If the synapse is complete, the naïve TCD4 cell will be
A

activated

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126
Q

will increase in size, divide and differentiate into clones of effector T-helper I & and T-helper II

A

TCD4

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127
Q

becomes effector t helper 1 in presence of

A

interleukin XII

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128
Q

becomes effector t helper 2 in presence

A

interleukin IV

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129
Q

i. Are the “commander in chief” of the immune system

A

Efffector T helper cells

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130
Q

produce lyphokines that facilitate the activation of naïve TCD8 cells, the maturation of effector T cytotoxic cells and the efficiency of macrophages

A

T helper 1

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131
Q

facilitate the activation of naïve B lymphocytes and the production of antibodies

A

T Helper II

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132
Q

produced by both helper I and helper II;
stimulates T helper cells and helps activate naïve TCD8 cells;
helps activates naïve B lymphocytes by binding to CD24 receptors

A

Interleukin II

133
Q

encourages activated B cells to stop multiplying, differentiate into plasma cells and start producing antibodies (produced by Helper II)

A

B cell growth factor

BCGF

134
Q

= instructs B cells to stop multiplying, differentiate into plasma cells and start producing antibodies (produced by helper II)

A

B cell differentiation factor

BCDF

135
Q

= helps activate T cytotoxic cells, increases the ability of plasma cells to produce antibodies, keeps macrophages at the site of an infection and helps them digest the cells they have engulfed, stimulates suppressor cells (produced by helper I and helper II)

A

=Gamma interferon

136
Q

i. TCD4 cells that produce inhibitory lymphokines that help call off an adaptive immune response when the antigen (microbe) that elicited the immune response has been eliminated

A

Regulatory (Suppressor T cells)

137
Q

i. Long lived cells that are the result of affinity maturation

A

Memory T Helper cell

138
Q

develop from lymphoid stem cells that differentiate into naïve cells in the bone marrow

A

B cells

139
Q 
acquire Ig (immunoglobulin) or class IgD antibody receptors and
ii.	Undergo positive and negative selection to become
A

B cells

140
Q

from the bone marrow, each distinguished from the others by its unique

A

Ig receptor

141
Q

c. Naïve B cells migrate to lymphoid tissue and areas frequented by microbes

A

i. Near the skin

ii. Lining of the digestive tract etc where they await activation

142
Q

i. B cells become activated when their ___ receptors interact directly with epitopes on the surface of whole, free antigens e.g. viruses or bacteria

A

Ig

143
Q
  1. The B cell uses its Ig receptor to bind to and ingest the microbe
    a. The microbe is processed into epitopes which are
    b. Presented to T helper II cells by B cell
    ____
A

MHC II receptors

144
Q
  1. T helper cells use their T cell receptors to examine the MHC II epitope complexes and if its receptor recognizes a ___
A

complementary epitope

145
Q
  1. The T helper begins to produce the co stimulatory molecule ___ II which binds to the B cell ___
A

Interleukin II

B cell CD24 receptors

146
Q

Recognition of the epitope plus co stimulation by ___ starts the activation of the B cell

A

Interleukin II

147
Q
  1. The T helper cell subsequently produces BCGF, BCDF, interleukin IV, and gamma interferon to orchestrate the development of naïve B cells into ___ and ___
A

memory cells and plasma cells

148
Q

=effector B cells

A

plasma cells

149
Q

cells secrete antibodies (humoral immunity), protein recognition molecules

A

plasma cells

150
Q

=used as B cell receptors

A

IgD

151
Q

are the first to be produced, but can’t pass through the placenta

A

IgM

152
Q

appear later in primary immune response as result of class switching; most common antibodies and can pass through the placenta

A

IgG

153
Q

= produced when plasma cells located in mucous membranes and mammary glands class switch; found in mother’s milk

A

IgA

154
Q

normally attacks parasitic worms; allergies if attach to mast cells and basophils

A

IgE

155
Q

b. Bind to “Free’ antigens, marking them for destruction by WBC’s

A

Antibodies

156
Q

reactions where the antibodies bind to and block the activity of a virus, toxin, or enzyme; immobilized antigen is then eaten by WBCs or may deteriorate on its own (toxins will have a half life)

A

Neutralization

157
Q

reactions where antibodies link soluble antigen molecules (toxins enzymes) making them insoluble and precipitate out of solution

A

Precipitation

158
Q

when bacteria, coated with antibodies are more easily consumed by WBC’s

A

iii. Opsonization

159
Q

reactions where antibodies link foreign cells to one another

A

iv. Agglutination

160
Q

when complement reacts with antibody bound microbes; leads to microbe lysis, phagocytosis of cellular antigens and/or inflammation

A

v. Complement fixation

161
Q

i. Can rapidly become plasma cells during a subsequent immune challenge

A

c. Memory B cells

162
Q
  1. Are associated with the cell membrane of all nucleated cells of the body
  2. Intracellular surveillance (cell infected or cancerous)
A

MHC 1

163
Q
  1. Associated with the cell membrane of macrophages, B Lymphocytes and dendritic cells
  2. When enzymes break down phagocytized antigens into epitopes, the peptides are transported to the cell surfaced attached to these receptors
A

MHC II

164
Q
  1. T cells

2. Recognizes ONE specific antigen

A

T cell receptor

165
Q
  1. B cells

2. Bind to “Free’ antigens, marking them for destruction by WBC’s

A

B cell receptor = IG

166
Q
  1. T cells

2. attachment receptors that help T cells bind to MHC II-epitope complexes

A

CD4

167
Q
  1. Other T cells have this receptor

2. receptors are attachment receptors that help T cells bind to MHC I-epitope complexes

A

CD8

168
Q
  1. Dendritic cells

2. Co-stimulatory molecule that binds to CD28 on T cells, confirms that antigen presented is not normal.

A

B7

169
Q
  1. Dendritic cells
  2. If receptor have been activated (bound to antigens recognized as dangerous, e.g. flagellin), the dendritic cells will display other co-stimulatory molecules
A

Toll-like

170
Q
  1. The T helper begins to produce the co stimulatory molecule Interleukin II which binds to the B cell ___ receptors
  2. Recognition of the epitope plus co stimulation by Interleukin II starts the activation of the B cell
A

CD24

171
Q
  1. T cells

2. Get a costimulatory receptor

A

CD28

172
Q

i. Has a long latent period (about a week) during which naïve cells are activated and become effector cells
ii. Because of the delay, a person will become sick

A

primary immune response

173
Q

i. Has no significant delay
ii. Is based on memory cells
iii. Is much bigger/aggressive and
iv. Should keep a person from ever expressing disease signs or symptoms

A

b. Secondary = anamnestic immune response (Anamnestic = “without forgetting”)

174
Q

i. Consists of the protective mechanical barriers, phagocytes, and chemical with which you are born

A

Innate immunity

175
Q
  1. Occurs when a “wild type” antigen (microbe) you encounter stimulates an adaptive immune response where
A

Active

Naturally Acquired Immunity

176
Q
  1. You generate your own antibodies, effector cells and memory cells (and probably get sick)
A

Active

Naturally Acquired Immunity

177
Q
  1. Improves with the number of times you are exposed to the same antigen as memory cells increase in number and become more efficient
A

Active

Naturally Acquired Immunity

178
Q
  1. There’s no actual exposure to an antigen, no immune response, and no development of memory cells
A

Passive

Naturally Acquired Immunity

179
Q
  1. When a fetus or infant acquires antibodies from their mother via the placenta (igG) and /or her milk (igA) and is temporarily protected (antibodies have a half-life and eventually disappear
A

Passive

Naturally Acquired Immunity

180
Q
  1. Occurs when a person is immunized with a dead or living (attenuated) microbe, epitopes from a microbe or microbe products such as toxins
A

Active

Artificially Acquired Immunity

181
Q
  1. A primary injection results in an adaptive immune response that ultimately generates memory cells
A

Active

Artificially Acquired Immunity

182
Q
  1. Later, when the person actually encountes the living, “Wild” microbe or its products, memory cells quickly differentiate into effector cells which initiate a rapid, dramatic anamnestic response and another generation of even more effective memory cells
A

Active

Artificially Acquired Immunity

183
Q
  1. A preventative technique that protects the individual against future encounters with a dangerous microbe
A

Active

Artificially Acquired Immunity

184
Q
  1. Antibodies are provided by another person/animal
A

Passive

Artificially Acquired Immunity

185
Q

i. Due to age (very young, elderly)
ii. Due to malnutrition
iii. Due to treatments: chemo/radiation therapy, anti-transplant rejection drugs
iv. Due to diseases that depress/destroy the immune response, e.g. AIDS

A

Reduced immunity

186
Q
  1. Microbes gain a stable foothold at the portal of entry;

2. Dependent on binding between specific molecules on host and pathogen

A

Adhesion

Attachment

187
Q

a. Fimbriae
i. G+/G- to help stick to you
b. Flagella
c. Glycocalyx
i. Sticky
ii. Slime layer
d. Cilia
e. Suckers
f. Hooks
g. Barbers

A

Adhesian Attachment

188
Q

a. Produced by some fungi (see ringworms) and digests the keratin in skin

A

Keratinase

189
Q

a. Digests hyallyronic acid, an intracellular cementing substance between surface cells

A

Hyaluronidase

190
Q

a. Enzyme that digests collagen, the most common protein in the body (CT)

A

Collagenase

191
Q

a. Convert plasminogen into plasmin

b. Enzymes that breaks down blood clots

A

Streptokinase/Staphylokinase

192
Q

causes a web-like clot that impedes WBC movement

A

Coagulase

193
Q

a. Kills WBC’s

A

Leukocidin

194
Q

a. Mechanically inferfere with phagocytosis

A

Fimbriae and Capsules

195
Q

a. May inhibit digestion by phagocytes

A

Resistance cell walls

196
Q

a. Are toxins that act as pores
b. Lyse red blood cells
c. Iron released from RBCs is appropriated for microbial use
d. Alpha’s cause partial hemolysis leaving a greenish ring around microbial colonies
e. Beta’s cause complete hemolysis leaving a clear ring around microbial colonies

A

Hemolysins

197
Q
  1. Hemolysins

Viruses enter host cells and take over the resources and machinery of their hosts

A

Acquisition of host resources

198
Q

i. Are the lipid A part of the outer membrane of Gram Negative bacteria
ii. Are released when gram negative bacteria die

A

Endotoxin

199
Q

iii. Are weak, non specific and cause a fever

iv. Stimulate weak immunity

A

Endotoxin

200
Q

v. Are stable
1. Cannot be denature and converted into a toxoid
2. Can’t be used for immunization

A

Endotoxin

201
Q

i. Are associated with a few gram positive and a few gram negative bacteria
ii. Are secreted

A

exotoxin

202
Q

iii. Are polypeptides, unstable, powerful, do not tend to cause fever, and stimulate strong immunity
iv. Can be denatured and converted to a toxoid which can be used for immunization

A

exotoxin

203
Q

v. Highly specific
1. Neurotoxins
Enterotoxins

A

exotoxin

204
Q

a. Attack nervous system
i. Botulin
ii. Tetanospasmin

A

Neurotoxin

205
Q

a. Attack organs of the digestive tract
i. Shiga toxin
ii. Cholera toxin

A

Enterotoxins

206
Q

i. Clostridium botulinum

A

Botulism

207
Q
  1. Normally and intoxication (toxin is consumed via contaminated food)
A

Botulism

208
Q
  1. Endospores consumed by an infant (infant botulism)
A

Botulism

209
Q
  1. Endospores introduced into a wound
A

Botulism

210
Q
  1. Exotoxin/neurotoxin
A

Botulism

211
Q

a. Toxin carried to neuromuscular junctions and blocks Ach release
b. Causes Flaccid paralysis

A

Botulism

212
Q

c. Blocks release of neurotransmitter Acetylcholine, which stimulates skeletal and smooth muscle to contract

A

Botulism

213
Q
  1. Paralysis of muscles, including muscles of inspiration
A

Botulism

214
Q

iv. Treatment
1. Support
2. Antitoxins
3. Antibiotics (wound)

A

Botulism

215
Q

v. Prevention
1. Properly prepare food to destroy endospores
2. Avoid feeding honey/corn syrup to infants under age of 2 (associated w/SIDS)

A

Botulism

216
Q
  • Hemorrhagic colitis = hemolytic uremic syndrome
A

=shiga toxin

217
Q

i. Both caused by Escherichia coli O157:H7

A

=shiga toxin

218
Q
  1. Emerged in 1975

2. First detected in 1982 and is now leading cause of acute kidney failure in children

A

=shiga toxin

219
Q
  1. Outbreaks include 2 outbreaks in 1992 (including Jack-in-the-Box outbreaks in Washington)
A

=shiga toxin

220
Q
  1. Transmission

a. Primarily through ground beef, leafy green and unpasteurized beverages

A

=shiga toxin

221
Q

b. Can be person to person in households, daycare centers and other institutions

A

=shiga toxin

222
Q

iii. Lysogenizes via a viral prophage –> shiga toxin (exotoxin)

A

=shiga toxin

223
Q
  1. Binds to receptors
    a. On cells lining small blood vessels
    b. That are more common in children than adults
A

=shiga toxin

224
Q
  1. Enters cells and
    a. Inactivates ribosomes
    b. Stops protein production
A

=shiga toxin

225
Q
  1. Cells die
    a. Break down of vessel lining –> blood clots and/or hemorrhage
    b. Digestive tract –> hemorrhagic colitis (bloody diarrhea)
A

=shiga toxin

226
Q
  1. Cells die
    a. Kidney glomeruli
    i. Kidney failure
    ii. Hemolytic Uremic Syndrome
  2. ~3000 cases/year
A

=shiga toxin

227
Q

iv. Treatment
1. Support
2. No antibiotics
a. dead cells release lipid A
b. antibiotics activate prophage leading to more toxin production

A

=shiga toxin

228
Q

v. Prevention
1. Cook your food
2. Avoid ground beef, leafy greens and unpasteurized beverages

A

=shiga toxin

229
Q

i. Vibrio cholerae
ii. Bengal cholera is a new, virulent strain and
iii. Threatens to become the world’s 8th cholera pandemic since 1837

A

cholera toxin

230
Q

iv. Spread via salt water

v. Exotoxin

A

cholera toxin

231
Q

a. Binds to cell receptors lining the intestines

b. Chloride and bicarbonate ion channels open

A

cholera toxin

232
Q
  1. Sodium follows the chloride out of the cell, water follows salt
A

cholera toxin

233
Q

a. Creates salt water environment for the bacteria

b. Resultant diarrhea (rice water stools) assists transmission of the bacteria

A

cholera toxin

234
Q

vi. Treatment

1. Re-hydration therapy

A

cholera toxin

235
Q

vii. Prevention

1. Clean water (4 layers of sari cloth removes 99% of microbes from water in India)

A

cholera toxin

236
Q

i. Prevention
1. Vaccine evaluated in Africa (2003) is 90% effective
a. Need for cold chain distribution
b. Short shelf life
c. High cost 7-12$
d. Multiple doses

A

cholera toxin

237
Q

viii. Stimulation of extreme host responses
1. Extreme inflammation
2. Abscess formation
3. Inappropriate blood clotting

A

cholera toxin

238
Q

ix. Evasive strategies
1. Depression of the immune response
2. High mutation rate
3. Intracellular
4. Triggering an autoimmune response
5. Mimicking host molecules
6. Formation of biofilms

A

cholera toxin

239
Q

i. Tetanus = Clostridium Tetani

A

Tetanospasmin

240
Q

ii. Transmission
1. Inoculation
2. Cutting umbilical cord with dirty knife (70,000 infant African deaths/year)

A

Tetanospasmin

241
Q

iii. Virulence factor

1. Tetanospasmin

A

Tetanospasmin

242
Q

a. Exotoxin
b. Neurotoxin
c. 1 of 3 most powerful toxins known

A

Tetanospasmin

243
Q

d. Follows nerve to spinal cord and brainstem

e. Inhibits release of inhibitory neurotransmitters glycine (spinal cord) and GABA (brain stem)

A

Tetanospasmin

244
Q

f. There is an increase in number of impulses sent to the skeletal muscle
g. Muscle spasms
i. Lock jaw
ii. Muscles of inspiration becomes non-functions –> breathing stops

A

Tetanospasmin

245
Q

iv. Treatment
1. Support
2. Antitoxin
3. Antibiotic
4. Muscle relaxants while anon terminal re-grows

A

Tetanospasmin

246
Q

v. Prevention
1. Toxoid vaccine (denatured tetanospasmin)
a. DTaP (children <6)
b. Tdap (adolescent and adult 1 time booster)
c. Td booster every 8-10 years

A

Tetanospasmin

247
Q

i. Agent must be isolated from host displaying the disease, grown in pure culture and characterized by testing

A

Koch’s postulates

248
Q

ii. When the agent from the pure culture is inoculated into susceptible hosts, it must cause the disease

A

Koch’s postulates

249
Q

iii. The agent must be re-isolated from the diseased host and identified as the original specific causative agent

A

Koch’s postulates

250
Q

iv. A specific causative agent must be observed in every case of a disease.

A

Koch’s postulates

251
Q
  1. Disease has a rapid development and course
A

Acute

252
Q
  1. Diseases which are slow and persistent
A

Chronic

253
Q
  1. Diseases have periods of inactivity between attacks

2. Herpes

A

Latent

254
Q
  1. Diseases are confined to a specific area

2. Giardia in intestines

A

Localized

255
Q
  1. When infectious agent breaks loose from a local infection and carried to other tissues
  2. Tetanus
A

Focal

256
Q
  1. Microbes or their products are In the blood
A

Sepsis

257
Q

a. Bacteria and viruses are present in the blood, but don’t multiply

A
  1. Bacteremia and viremia
258
Q

a. Toxins are in the blood

A

Toxemia

259
Q
  1. Microbes are present and multiply in the blood

2. Malaria

A

Septicemia

260
Q
  1. Diseases affect the entire body
A

systemic

261
Q
  1. Diseases represent an initial infection
A

Primary

262
Q
  1. Diseases represent an infection that follows a primary infection, usually as the result of the patient having been weakened by the primary disease
A

Secondary

263
Q
  1. The time between infection and the appearance of signs and/or symptoms
A

Incubation period

264
Q
  1. The short period of time when non-specific symptoms appear (the effects of interleukin-I)
A

prodromal

265
Q
  1. The period when the disease develops signs and symptoms characteristic of the disease
A

Invasive

266
Q
  1. Critical stage

2. The period of the most intense symptoms

A

Acme

267
Q
  1. Host immune response begins killing the pathogen

2. Symptoms characteristic of the disease begin to decrease

A

Decline

268
Q
  1. The recovery phase when tissues repair and healing takes place
  2. No symptoms of the disease, but microbes may still be present
A

Convalescence

269
Q

i. Selective agents
ii. Artificial passive immunization
iii. Boosting host defense mechanisms
iv. Reduce symptoms
v. Vaccine

A

Treatment for infectious diseases include

270
Q
  1. Antibiotics
  2. Antivirals
  3. Sulfa drugs
A

Selective agents

271
Q
  1. Homologous pooled human antibody- gamma globuins
  2. Homologous human yperimmune globulins
    a. Convalescent serum
    b. Diptheria – 1st disease cured 1891
  3. Heterologous hyperimmune serum
    a. Antitoxin
    b. Neutralizing antibodies
A

Artificial passive immunization

272
Q
  1. Administering gamma interferon
  2. Use of interleukin II
  3. Good nutrition
A

Boosting host defense mechanisms

273
Q
  1. Aspirin
  2. Fluids
  3. Etc.
A

Reduce symptoms

274
Q

i. Good nutrition
ii. Good sanitation
iii. Artificial active immunization
iv. Eliminate non human vectors
v. Treat carriers
vi. Good surveillance
vii. Quarantine

A

Prevention of Diseases include

275
Q
  1. Provides herd immunity
  2. Long term
  3. Stimulates B and T cell formation and differentiation
A

Artificial active immunization

276
Q

a. Developed first natural vaccine for smallpox

i. Variola major and minor

A

Jenner

277
Q

i. Small pox killed 1 in 3 (500 million victims during 20th century)
ii. Variolation

A

Small pox

278
Q
  1. Used to prevent serious smallpox infections (person inoculated with Variola from a mild case of smallpox)
    iii. Jenner, first “natural” vaccine based on Cowpox virus (vaccination)
  2. Live virus grown on skin of calves
  3. Arm to arm
A

small pox

279
Q

a. Hybrid mix of cowpox and smallpox viruses

b. 1 dose of dried calf lymph

A

Dryvax

280
Q

a. Smallpox eradicated – herd immunity
b. DNA virus, no mutations
c. NO question who was infected

A

1979

281
Q

a. Discovered principle behind vaccinations

b. 1st laboratory developed a vaccines for rabies and anthrax

A

Pasteur

282
Q
  1. Italian for 40 days

2. First attempted in 14th century Venice to stop Bubonic plague; ships remained at anchor for 40 days

A

Quarantine

283
Q

a short term increase (from months to years) in the incidence of a specific microbial disease in a limited population (confined in time and space)

A

=epidemic

284
Q
  1. 1849

2. Traced a cholera outbreak to a water pump

A

John Snow

285
Q
  1. Is the number of new cases of a disease seen in a specific time period
A

Incidence

286
Q
  1. Corresponds to the number of people infected with a specific microbe at any one tme.
A

ii. Prevalence

287
Q
  1. Number of deaths per population at risk
A

Mortality rate

288
Q
  1. Disease must be communicable from person to person

2. Each host must spread the disease to at least two other people

A

Propagated epidemic

289
Q
  1. Usually begins with an index case

a. =the first person to bring a disease into a community

A

Propagated epidemic

290
Q
  1. When multiple hosts come in contact with the same microbe source
  2. The disease may not be communicable
    a. Everyone eats same potato salad or water
A

Common source epidemic

291
Q

a. Corresponds to the length of the incubation period
b. Is when the disease is asymptomatic
c. The microbe can be spread during this phase

A

Latent (lag) phase

Phases of epidemic disease transmission

292
Q

a. Corresponds to rapid transmission of the disease
b. Depends upon the number of contacts made by contagious individuals
c. Continues until a high percentage of the population has encountered the organism and the number of new cases begins to decline

A

Logarithmic phase

Phases of epidemic disease transmission

293
Q

a. Is when there is low incidence (few new cases are reported) and some of the population have started to recover (or have died)
b. Is when antibodies are building in the population

A

Stationary phase

Phases of epidemic disease transmission

294
Q

a. When few new cases appear

A

Decline phase

Phases of epidemic disease transmission

295
Q

a. If a population is small and the host is not motile, the epidemic will disappear

A

Epidemic aftermath

296
Q

the disease spreads to at least two continents

A

Pandemic disease

297
Q

a disease persists in a population

A

Endemic disease

298
Q

ii. The population must be threshold for a disease

A

Endemic disease

299
Q

iv. An endemic disease usually becomes a childhood disease

v. Controlled by vaccines (reduces the number of susceptible people)

A

Endemic disease

300
Q

iii. Be large enough that it can continuously generate susceptible people
1. Enough children are born to keep the disease spreading

A

Endemic disease

301
Q
  1. A population’s cultures
  2. What percent of apopulation is disadvantaged, e.g. have poor sanitation and few medical services available
  3. Is the population disrupted (war etc.) such that there are reduced medical services
  4. Is there crowding
  5. The present herd immunity of the population
A

Population factors

302
Q
  1. Is the climate hot vs. cold
  2. Is there pollution
  3. Is there proximity to emerging microbes
A

Environmental factors

303
Q
  1. How virulent is the strain of microbe e.g. does it generate symptoms that encourage the microbes spread: severe diarrhea
  2. What is the incubation period of the microbe
  3. How contagious is the microbe
A

Microbial factors that influence an epidemic

304
Q

b. The longer the incubation period,

A

the greater the risk for generating an epidemic (the disease has more time to spread before it’s detected)

305
Q

c. The shorter the incubation period,

A

the more rapidly a person gets sick and stays home, reducing the microbe spread and the risk of an epidemic

306
Q

a. Are spread person to person or by fomites

b. Enter the body via skin and mucous membranes

A

direct contact disease

307
Q

c. Are caused by microbes that
i. Are sensitive to drying and temperature variation
ii. Are associated with capsules and pus formation
iii. Produce toxins, enzyme, etc. that the microbe uses to invade
iv. Stimulate an immune response only if the microbe contacts cells of the immune system

A

direct contact disease

308
Q

a non living object which transmit the microbe, but on which the microbe cannot multiply

A

=fomites

309
Q

a. Enter the body via the mouth
b. Are influenced by a dilution factor
c. Feces are the usual source of contamination
d. The pathogen is usually an intestinal G- negative rod
e. Prevention will increasingly depend upon controlling contamination of feed and water and animals themselves

A

Food and waterborne diseases

310
Q

i. The greater dilution of microbes in water generates a long incubation with few cases of the disease appearing

A

ii. Less dilution by food generates a shorter incubation period and more cases of the disease

311
Q

i. Usually have animal reservoirs
ii. Contamination tends to occur early in the production process
iii. Centralized production and wide distribution of products encourages widespread epidemics

A

feces source of contamination

312
Q

i. Beef
ii. Poultry
iii. Etc.

A

Prevent - avoid these things

313
Q

a. Enter the body via the inhalation of droplets, dust, dry skin or spores
b. Involve microbes that are the least susceptible to drying

A

Airborne disease

314
Q

a. May be influenced by a dilution factor

b. The route of transmission most closely associated with epidemics

A

Airborne disease

315
Q

i. The greater dilution of microbes outdoor reduces exposure to the microbe

A

ii. The reduced dilution indoors explains the need for good ventilation and dust control to reduce the spread of airborne diseases

316
Q

a. May involve a vector or fomite
b. Usually stimulate good immunity
c. Not typically associated with epidemics

A

Inoculation diseases

317
Q
  1. Are the sum of all constant sources of the microbe – include places where microbes replicate in nature (water, soil, animals, humans)
A

Reservoirs

318
Q

a. Are diseases acquired in a hospital or other medical facility

A

nosocomial infections

319
Q

i. During the 60’s and 70’s, Gram negative bacteria were the leading cause
ii. Gram + bacteria have emerged as the leading cause, eg.g. MRSA, VRE, and Clostridium difficile

A

nosocomial infections

320
Q

c. Transmission of these diseases include
i. Invasive procedures involving individuals in an already weakened state (increasing numbers of imunodeficient patients)
ii. Person to person contact
iii. Contact with contaminated equipment
iv. Airborne

A

nosocomial

321
Q

d. Often involve resistant microbes

A

nosocomial

322
Q

i. Hand washing and/or hand sanitizers
ii. Sterilizing equipment etc
iii. Controlling the generation of antibiotic resistant microbes

A

nosocomial

323
Q

something alive that transmit a disease

A

vectors

324
Q

i. An animal that transmits the disease microbe from one host to another

A

animal vector

325
Q

ii. Usually involves inoculation

1. E.g. mosquitos and ticks

A

animal vector

326
Q
  1. Diseases that can be transmitted to humans from animals
A

zoonoses

animal vector

327
Q

i. A human that transmits disease

ii. May never have signs or symptoms of the disease

A

carriers=human vectors

328
Q
  1. The individual is colonized
  2. Most transmissions occurs during the incubation period of the disease or during convalescence
  3. Can transmit disease via all routes of transmission
A

human carriers

329
Q
  1. Increase the population’s resistance to diseases
  2. Reduce the number of reservoirs and vectors
  3. Be sure hospitals are using aseptic techniques and provide dust control and ventilation
  4. Encourage people to WASH THEIR HANDS/sanitize
  5. Increase the number of health networks to provide better suveillance
A

Prevention of Epidemics

Microbio (14 decks)

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