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HLSC 222 > Ch.8 > Flashcards

Ch.8 Flashcards

1
Q

Communicability

A

Ability to spread from one individual to others and cause disease

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2
Q

Infectivity

A

-Pathogen ability to invade and multiply
-Involves attachment, escape of phagocytes, and dissemination (Spread)

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3
Q

Virulence

A

Severity or harmfulness of disease or poison

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4
Q

Toxigenicity

A

Ability to produce toxins
(Greatly influence pathogens virulence)

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5
Q

Portal of entry

A

Route of which a pathogen infects host
-Direct contact/inhalation/ingestion
-Bites of an animal or insect

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6
Q

Bacteria

A

-Prokaryotes
-Aerobic or anaerobic
-Gram+ or Gram-

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7
Q

Prokaryotes

A

lack a discrete nucleus

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8
Q

Staphylococcus aureus

A

-Life threatening
-Major cause of nosocomial disease

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9
Q

Staphylococcus aureus is found

A

On normal skin and nasal passages

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10
Q

Virulent abilities of Staphylococcus aureus

A
  1. Produce protein that blocks compliment attack
  2. Avoid innate immunity
  3. Resist lysosome when phagocytized
  4. Resist many antibiotics actions
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11
Q

How does Staphylococcus aureus avoid innate immunity

A

producing inhibitors that avoid recognition

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12
Q

How does staphylococcus aureus resist lysosome

A

changing the chemistry of their cell walls

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13
Q

Toxins produces by bacterial diseases

A

-Endotoxins
-Exotoxins

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14
Q

Exotoxins

A

-Released from within pathogen
-Enzymes damage host cell plasma membranes or inactivate protein synthesis

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15
Q

Endotoxins

A

-Released from outer capsule
-Activate inflammatory responses and produce fever

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16
Q

Bacteremia (presence) or septicemia (growth)

A

Result of defense mechanism failure

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17
Q

Endotoxins: inflammatory response

A

-Activate compliment clotting systems
= increased capillary permeability
=large volumes of plasma into surrounding tissues
= results in hypotension

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18
Q

Viral disease

A

most common affliction of humans

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19
Q

Viral replication

A

requires entry into host cell

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20
Q

Virus structure

A

DNA/RNA surrounded by capsid and possibly an envelope

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21
Q

Viruses are

A

Self-limiting
-Require a host to survive

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22
Q

Viral transmission

A

-Aerosol
-infected blood
-sexual contact
-Vectors

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23
Q

Vectors

A

ticks, mosquitos, etc

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24
Q

Cytopathic effects of viruses

A

-Inhibit cell DNA/RNA synthesis
-release of lysosomes into host cell
-Fusion of host cells
-Alteration of host cells antigens properties
-Transform host into cancerous cells
-Utilizes host cells resources

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25
Q

Viral release of lysosomes causes

A

cell death

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26
Q

Alteration of host cells antigens properties =

A

immune system attacks own cells

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27
Q

Transforming host cells into cancerous cells =

A

uninhibited growth

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28
Q

Cytopathic

A

causing damage to living cells

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29
Q

Influenza

A

Highly contagious viral infection of respiratory passages

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30
Q

Antigenic variation

A

Ability to change antigen (spikes) yearly

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31
Q

Antigenic variation process

A

-Antigens utilized to activate adaptive immune response

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32
Q

Ability to change antigen =

A

Dysfunction adaptive immune responses (B/T cells)

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33
Q

SARS-CoV-2 Virus

A

Responsible for COVID-19

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34
Q

Fungus

A

-Large eukaryotes with thick, rigid cell walls
-Single cell yeasts, multicell molds, or both

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35
Q

Why can fungi resist penicillin

A

Penicillin was made from fungi (Molds)

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36
Q

Fungus reproduction

A

-Simple division
-Budding

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37
Q

Mycoses

A

disease caused by fungi

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38
Q

Dermatophytes

A

fungi that invade skin, hair, or nails

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39
Q

Disease caused by dermatophytes

A

diseases are called “Tineas”
-Eg. tinea capitis (scalp)

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40
Q

Fungal pathogenicity

A

-adapts to host environment
-suppress immune defenses
-low WBC count promotes fungal infection

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41
Q

How can fungi adapt to host environment

A

-Wide temp variations
-low oxygen needs

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42
Q

Most common fungal infection

A

Candida albicans

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43
Q

Candida albicans location

A

-Skin microbiome
-GI tract
-vagina

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44
Q

Who are most effected by fungal infections

A

-Cancer pts
-Transplant pts

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45
Q

Disseminated (spreading) of fungal infections in immunocompromised

A

-Deep infections
-High mortality rates

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46
Q

Mortality of Candidiasis

A

30-40%

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47
Q

Parasitic infections cause

A

-unicellular protozoa
-large worms (helminths)
-eg. flukes, nematodes, tapeworms

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48
Q

Parasitic infection spread

A

-Vectors
-contaminated food or water

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49
Q

Plasmodium vivax

A

malaria

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50
Q

malaria

A

occurs in RBC

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51
Q

Malaria process

A

Continual infection of RBC
-anemia in 48-72h
-RBC release cytokines (TNF-a/IL-1)

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52
Q

Malaria symptoms

A

-fever
-chills
-vomiting

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53
Q

Counter measures

A

-Antibiotics
-Antimicrobials

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54
Q

Antibiotics

A

natural products of fungi, bacteria, or other microorganisms that affect the growth of specific microorganisms

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55
Q

Antimicrobials

A

-Bactericidal
-Bacteriostatic

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56
Q

Bactericidal

A

agent that kills other microorganisms

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57
Q

Bacteriostatic

A

agent inhibits growth of other microorganisms

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58
Q

Cidal means

A

Kill

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59
Q

Safeguards to infections

A

known but poorly implemented

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60
Q

Safeguards

A

-Hand hygiene
-proper sanitary disposal
-water treatment/prevent contamination
-sanitary food transportation, preparation, serving
-control of vectors
-support research

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61
Q

How to control vectors

A

-draining standing water
-mosquito eradication programs

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62
Q

1944

A

Penicillin effective at treating infection in British hospital

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63
Q

1946

A

14% of all Staphylococcus aureus are penicillin resistant

64
Q

1950

A

59% resistant

65
Q

1990

A

89% resistant

66
Q

What caused antibiotic resistance

A

-Lack of compliance
-Overuse

67
Q

Lack of compliance with therapeutic regimen

A

-Not using antibiotic for prescribed duration

68
Q

Result of antibiotic resistance

A

Strongest microbes are left alive = repopulation with pathogens resistant to specific antibiotics

69
Q

Overuse of antibiotics

A

Destruction of normal microbiomes = opens more space for more infectious/resistant pathogens

70
Q

Vaccines

A

-Biological preparation of weakened (attenuated) or dead (inactivated) pathogens

71
Q

Benefits of vaccines

A

-Adaptive response
-2 week immune response to non-viral pathogen

72
Q

HERD immunity

A

Requires 85% of population to be immunized

73
Q

Result of vaccine

A

when infection by viral pathogen occurs, Adaptive Immunity already prepared (No 2w delay)

74
Q

Adaptive response

A

requires 2w to activate

75
Q

Vaccine allows

A

2w period to be performed against a non-viral pathogen

76
Q

Vaccine mixture

A

DTaP vaccine
-Diphtheria
-Tetanus
-Pertussis

77
Q

Toxoids

A

chemically altered pathogen toxin injected = allows body to learn to defeat pathogens toxin

78
Q

Passive Immunity

A

Performed antibodies (against pathogen) are given to individuals

79
Q

Performed Antibodies

A

-Human immunoglobulin
-Becoming focus after rise of antibiotic resistance

80
Q

Human Immunoglobulin

A

antibodies obtained from pathogen survivor

81
Q

Immune deficiencies

A

-Primary
-Secondary

82
Q

Primary are

A

genetic

83
Q

Secondary are

A

From another illness

84
Q

Primary Deficiencies

A

-Most from a single gene defect
-Mutations are sporadic and noni-inherited

85
Q

Primary deficiency mutations

A

-Occur before birth
-Symptoms show early or late in life

86
Q

_ in _ have a primary condition, _ undiagnosed

A

1, 200, 70%

87
Q

Primary are categorized into groups based off what part of the immune system they affect

A

-B + T lymphocytes
-Antibody deficient

88
Q

Combined deficiencies

A

-Severe combined deficiency
-DiGeorge Syndrome
-Hypogammaglobulinemia

89
Q

Severe combined deficiency

A

-Underdeveloped thymus = absence of T cells
-few detectable lymphocytes

90
Q

DiGeorge syndrome

A

-Thymus + Parathyroid dysfunction
-result in inadequate T cell production and management of plasma

91
Q

Hypogammaglobulinemia

A

-Result from defect in B cell maturation or functions
-Lower levels of circulating immunoglobulins (antibodies) in bloods

92
Q

Secondary deficiencies

A

-Acquired deficiencies
-More common then primary
-Most are less severe, except cancer and AIDS

93
Q

Evaluation of immunity

A

Complete blood count (CBC) with differential

94
Q

CBC

A

Total number of RBS, WBC, and platelets

95
Q

Differential

A

Individual numbers of lymphocytes, granulocytes, and monocytes

96
Q

Quantitative determination of immunoglobulins

A

Determines subpopulations of immunoglobulins

97
Q

Total complement assay

A

Total number of complements in blood

98
Q

Replacement therapies for immune deficiencies

A

-Stem cell
-Mesenchymal stem cell
-Gene therapy

99
Q

Stem cell transplantation

A

-From bone marrow, umbilical cord cells
-most cases are temporary

100
Q

Mesenchymal stem cell injection (MSCs)

A

-Undifferentiated stem cells found in bone marrow
-Under go differentiation into other cell types
-Have potential immunosuppressant properties

101
Q

Gene therapy

A

-2 girls received first therapeutic replacement of defective genes
-Inserted normal genes into their genetic material

102
Q

Result of gene therapy

A

reconstitution of immune system

103
Q

Caution of gene therapy

A

-Some recipients developed leukemia

104
Q

Acquired Immunodeficiency Syndrome (AIDs) cause

A

-by viral disease
-Human immunodeficiency virus (HIV)

105
Q

AIDS action

A

-Deletes helper T cells (Th cells)
-Unable to activate T + B cells

106
Q

HIV result

A

-dysfunctional adaptive immune system
-Increased susceptibility of disease
= AIDS

107
Q

AIDs Epidemiology

A

-Heterosexual activity is more common transmission
-Women constitute >50% of those infected

108
Q

How do kids develop HIV/AIDs

A

-Through contact with virus through moms placenta
-Breast feeding milk

109
Q

Difficulties with HIV vaccine development

A

-HIV genetically and antigenically variable
-individuals with HIV have high levels of antibodies but they aren’t protective
-If vaccine makes antibodies they may not function correctly

110
Q

Epidemeology

A

Branch of medicine that deals with incidence, distribution, and possible control of diseases

111
Q

Treatment of HIV

A

Antiretroviral therapy (ART)

112
Q

Retroviral

A

virus with RNA not DNA

113
Q

ART effects

A

-Entrance inhibitors
-reverse transcriptase inhibitors
-integrase inhibitors
-protease inhibitors

114
Q

ART is not

A

curative but death is significantly reduced

115
Q

Hypersensitivity

A

-Altered immunological response to an antigen that results in disease or damage to a host

116
Q

Hypersensitivity eg.

A

-Allergies
-Autoimmunity
-Alloimmunity

117
Q

Allergies

A

-harmful effects of hypersensitivity to environmental (Exogenous) antigens
-eg. bee pollen

118
Q

Autoimmunity

A

-Disturbance in immunological tolerance of self-antigens (immune doesn’t recognize own antigens)
-called autoimmune diseases

119
Q

Alloimmunity

A

immune reaction to tissues of another individual
-eg. transfusions, transplants, fetus during pregnancy

120
Q

Mechanisms of hypersensitivity

A

-Type I
-Type II
-Type III
Type IV

121
Q

Hypersensitivity mechanisms are

A

interrelated, often reactions include more then one type

122
Q

Immediate hypersensitivity reactions

A

reactions that occur in minutes-hours
-eg. anaphylaxis

123
Q

anaphylaxis

A

most rapid severe immediate reaction
- in minutes

124
Q

anaphylaxis symptoms

A

-pruritis
-erythema
-vomiting
-diarrhea
-breathing difficulties

125
Q

Pruritis

A

severe itching

126
Q

erythma

A

repatches on skin

127
Q

Delayed hypersensitive reactions

A

reaction occurring after several hours and are maximal several days later

128
Q

Type I: IgE mediated

A

-Mediated by IgE and products of mast cells(histamine)
-most common

129
Q

Type I initial exposure to allergen

A

-IgE binds to mast cell receptors
-person is considered “sensitized”

130
Q

Type I subsequent (re-exposure) exposure

A

-mast cells release cytokines I = hypersensitive reaction

131
Q

Type I affects

A

-Tissues with high mast cell counts
-Skin, GI, Pulmonary tract

132
Q

Atopic

A

individuals predisposed to developing allergies

133
Q

Atopic 1 parent

A

40% offspring will have allergies

134
Q

Atopic 2 parents

A

both parents have allergies 80% children will have

135
Q

Type II: Tissue Specific is also

A

Cytotoxic sensitivity

136
Q

Cytotoxic hypersensitivity

A

Antibody mediated destruction of healthy host cells

137
Q

Type II cytotoxic hypersensitivity

A

Immune reactions against a specific cell or tissue

138
Q

Type II immune reactions

A

tissue specific antigens because they attach only on plasma membranes of certain cells

139
Q

Type II hypersensitivity cell example

A

platelets- they have no antigens that can be found on any other type of cell

140
Q

5 mechanisms of type II begins

A

with antibody binding to tissue-specific antigens

141
Q

Cells are destroyed by

A

antibodies and complements

142
Q

5 mechanism types

A

-A
-B
-C
-D
-E

143
Q

Antibodies binding to cells

A

-activates complement system
-formation of membrane complex
-disintegration or rupture of cell

144
Q

A

A

Cell is destroyed by antibodies and complements

145
Q

B

A

Cell destruction through phagocytosis by macrophage

146
Q

Antibodies binding to cells

A

macrophage recognition of cell to be phagocytized

147
Q

C

A

Tissue damage caused by toxic products produced by neutrophils

148
Q

Soluble antigens (C)

A

form infectious agents or hosts own cells bind to cells surface

149
Q

Neutrophils are attracted then (C)

A

Release their granules into healthy cells to damage them

150
Q

D

A

Antibody-dependent cell-mediated cytotoxicity (ADCC)

151
Q

IgG antibodies bind to antigens attracting

A

Natural killer cells that release toxic substances that destroy cell

152
Q

E

A

Target cell malfunction
-doesn’t destroy cell but causes malfunction
-antibodies prevent cell interaction with normal molecules

153
Q

Type III Hypersensitivity

A

Antigen-antibody immune complexes are formed in circulation and later deposited into vessel walls or extravascular tissues

154
Q

Type IV Hypersensitivity

A

-No involvement of antibody/mediated T-cells

155
Q

Type IV

A

-Graft rejection
-Allergic reactions from poison ivy or metals = t cell activation
=macrophage activation
= tissue damage

HLSC 222 (9 decks)

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