Ch.8 Flashcards
1
Q
Communicability
A
Ability to spread from one individual to others and cause disease
2
Q
Infectivity
A
-Pathogen ability to invade and multiply
-Involves attachment, escape of phagocytes, and dissemination (Spread)
3
Q
Virulence
A
Severity or harmfulness of disease or poison
4
Q
Toxigenicity
A
Ability to produce toxins
(Greatly influence pathogens virulence)
5
Q
Portal of entry
A
Route of which a pathogen infects host
-Direct contact/inhalation/ingestion
-Bites of an animal or insect
6
Q
Bacteria
A
-Prokaryotes
-Aerobic or anaerobic
-Gram+ or Gram-
7
Q
Prokaryotes
A
lack a discrete nucleus
8
Q
Staphylococcus aureus
A
-Life threatening
-Major cause of nosocomial disease
9
Q
Staphylococcus aureus is found
A
On normal skin and nasal passages
10
Q
Virulent abilities of Staphylococcus aureus
A
- Produce protein that blocks compliment attack
- Avoid innate immunity
- Resist lysosome when phagocytized
- Resist many antibiotics actions
11
Q
How does Staphylococcus aureus avoid innate immunity
A
producing inhibitors that avoid recognition
12
Q
How does staphylococcus aureus resist lysosome
A
changing the chemistry of their cell walls
13
Q
Toxins produces by bacterial diseases
A
-Endotoxins
-Exotoxins
14
Q
Exotoxins
A
-Released from within pathogen
-Enzymes damage host cell plasma membranes or inactivate protein synthesis
15
Q
Endotoxins
A
-Released from outer capsule
-Activate inflammatory responses and produce fever
16
Q
Bacteremia (presence) or septicemia (growth)
A
Result of defense mechanism failure
17
Q
Endotoxins: inflammatory response
A
-Activate compliment clotting systems
= increased capillary permeability
=large volumes of plasma into surrounding tissues
= results in hypotension
18
Q
Viral disease
A
most common affliction of humans
19
Q
Viral replication
A
requires entry into host cell
20
Q
Virus structure
A
DNA/RNA surrounded by capsid and possibly an envelope
21
Q
Viruses are
A
Self-limiting
-Require a host to survive
22
Q
Viral transmission
A
-Aerosol
-infected blood
-sexual contact
-Vectors
23
Q
Vectors
A
ticks, mosquitos, etc
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
25
Viral release of lysosomes causes
cell death
26
Alteration of host cells antigens properties =
immune system attacks own cells
27
Transforming host cells into cancerous cells =
uninhibited growth
28
Cytopathic
causing damage to living cells
29
Influenza
Highly contagious viral infection of respiratory passages
30
Antigenic variation
Ability to change antigen (spikes) yearly
31
Antigenic variation process
-Antigens utilized to activate adaptive immune response
32
Ability to change antigen =
Dysfunction adaptive immune responses (B/T cells)
33
SARS-CoV-2 Virus
Responsible for COVID-19
34
Fungus
-Large eukaryotes with thick, rigid cell walls
-Single cell yeasts, multicell molds, or both
35
Why can fungi resist penicillin
Penicillin was made from fungi (Molds)
36
Fungus reproduction
-Simple division
-Budding
37
Mycoses
disease caused by fungi
38
Dermatophytes
fungi that invade skin, hair, or nails
39
Disease caused by dermatophytes
diseases are called "Tineas"
-Eg. tinea capitis (scalp)
40
Fungal pathogenicity
-adapts to host environment
-suppress immune defenses
-low WBC count promotes fungal infection
41
How can fungi adapt to host environment
-Wide temp variations
-low oxygen needs
42
Most common fungal infection
Candida albicans
43
Candida albicans location
-Skin microbiome
-GI tract
-vagina
44
Who are most effected by fungal infections
-Cancer pts
-Transplant pts
45
Disseminated (spreading) of fungal infections in immunocompromised
-Deep infections
-High mortality rates
46
Mortality of Candidiasis
30-40%
47
Parasitic infections cause
-unicellular protozoa
-large worms (helminths)
-eg. flukes, nematodes, tapeworms
48
Parasitic infection spread
-Vectors
-contaminated food or water
49
Plasmodium vivax
malaria
50
malaria
occurs in RBC
51
Malaria process
Continual infection of RBC
-anemia in 48-72h
-RBC release cytokines (TNF-a/IL-1)
52
Malaria symptoms
-fever
-chills
-vomiting
53
Counter measures
-Antibiotics
-Antimicrobials
54
Antibiotics
natural products of fungi, bacteria, or other microorganisms that affect the growth of specific microorganisms
55
Antimicrobials
-Bactericidal
-Bacteriostatic
56
Bactericidal
agent that kills other microorganisms
57
Bacteriostatic
agent inhibits growth of other microorganisms
58
Cidal means
Kill
59
Safeguards to infections
known but poorly implemented
60
Safeguards
-Hand hygiene
-proper sanitary disposal
-water treatment/prevent contamination
-sanitary food transportation, preparation, serving
-control of vectors
-support research
61
How to control vectors
-draining standing water
-mosquito eradication programs
62
1944
Penicillin effective at treating infection in British hospital
63
1946
14% of all Staphylococcus aureus are penicillin resistant
64
1950
59% resistant
65
1990
89% resistant
66
What caused antibiotic resistance
-Lack of compliance
-Overuse
67
Lack of compliance with therapeutic regimen
-Not using antibiotic for prescribed duration
68
Result of antibiotic resistance
Strongest microbes are left alive = repopulation with pathogens resistant to specific antibiotics
69
Overuse of antibiotics
Destruction of normal microbiomes = opens more space for more infectious/resistant pathogens
70
Vaccines
-Biological preparation of weakened (attenuated) or dead (inactivated) pathogens
71
Benefits of vaccines
-Adaptive response
-2 week immune response to non-viral pathogen
72
HERD immunity
Requires 85% of population to be immunized
73
Result of vaccine
when infection by viral pathogen occurs, Adaptive Immunity already prepared (No 2w delay)
74
Adaptive response
requires 2w to activate
75
Vaccine allows
2w period to be performed against a non-viral pathogen
76
Vaccine mixture
DTaP vaccine
-Diphtheria
-Tetanus
-Pertussis
77
Toxoids
chemically altered pathogen toxin injected = allows body to learn to defeat pathogens toxin
78
Passive Immunity
Performed antibodies (against pathogen) are given to individuals
79
Performed Antibodies
-Human immunoglobulin
-Becoming focus after rise of antibiotic resistance
80
Human Immunoglobulin
antibodies obtained from pathogen survivor
81
Immune deficiencies
-Primary
-Secondary
82
Primary are
genetic
83
Secondary are
From another illness
84
Primary Deficiencies
-Most from a single gene defect
-Mutations are sporadic and noni-inherited
85
Primary deficiency mutations
-Occur before birth
-Symptoms show early or late in life
86
_ in _ have a primary condition, _ undiagnosed
1, 200, 70%
87
Primary are categorized into groups based off what part of the immune system they affect
-B + T lymphocytes
-Antibody deficient
88
Combined deficiencies
-Severe combined deficiency
-DiGeorge Syndrome
-Hypogammaglobulinemia
89
Severe combined deficiency
-Underdeveloped thymus = absence of T cells
-few detectable lymphocytes
90
DiGeorge syndrome
-Thymus + Parathyroid dysfunction
-result in inadequate T cell production and management of plasma
91
Hypogammaglobulinemia
-Result from defect in B cell maturation or functions
-Lower levels of circulating immunoglobulins (antibodies) in bloods
92
Secondary deficiencies
-Acquired deficiencies
-More common then primary
-Most are less severe, except cancer and AIDS
93
Evaluation of immunity
Complete blood count (CBC) with differential
94
CBC
Total number of RBS, WBC, and platelets
95
Differential
Individual numbers of lymphocytes, granulocytes, and monocytes
96
Quantitative determination of immunoglobulins
Determines subpopulations of immunoglobulins
97
Total complement assay
Total number of complements in blood
98
Replacement therapies for immune deficiencies
-Stem cell
-Mesenchymal stem cell
-Gene therapy
99
Stem cell transplantation
-From bone marrow, umbilical cord cells
-most cases are temporary
100
Mesenchymal stem cell injection (MSCs)
-Undifferentiated stem cells found in bone marrow
-Under go differentiation into other cell types
-Have potential immunosuppressant properties
101
Gene therapy
-2 girls received first therapeutic replacement of defective genes
-Inserted normal genes into their genetic material
102
Result of gene therapy
reconstitution of immune system
103
Caution of gene therapy
-Some recipients developed leukemia
104
Acquired Immunodeficiency Syndrome (AIDs) cause
-by viral disease
-Human immunodeficiency virus (HIV)
105
AIDS action
-Deletes helper T cells (Th cells)
-Unable to activate T + B cells
106
HIV result
-dysfunctional adaptive immune system
-Increased susceptibility of disease
= AIDS
107
AIDs Epidemiology
-Heterosexual activity is more common transmission
-Women constitute >50% of those infected
108
How do kids develop HIV/AIDs
-Through contact with virus through moms placenta
-Breast feeding milk
109
Difficulties with HIV vaccine development
-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
Epidemeology
Branch of medicine that deals with incidence, distribution, and possible control of diseases
111
Treatment of HIV
Antiretroviral therapy (ART)
112
Retroviral
virus with RNA not DNA
113
ART effects
-Entrance inhibitors
-reverse transcriptase inhibitors
-integrase inhibitors
-protease inhibitors
114
ART is not
curative but death is significantly reduced
115
Hypersensitivity
-Altered immunological response to an antigen that results in disease or damage to a host
116
Hypersensitivity eg.
-Allergies
-Autoimmunity
-Alloimmunity
117
Allergies
-harmful effects of hypersensitivity to environmental (Exogenous) antigens
-eg. bee pollen
118
Autoimmunity
-Disturbance in immunological tolerance of self-antigens (immune doesn't recognize own antigens)
-called autoimmune diseases
119
Alloimmunity
immune reaction to tissues of another individual
-eg. transfusions, transplants, fetus during pregnancy
120
Mechanisms of hypersensitivity
-Type I
-Type II
-Type III
Type IV
121
Hypersensitivity mechanisms are
interrelated, often reactions include more then one type
122
Immediate hypersensitivity reactions
reactions that occur in minutes-hours
-eg. anaphylaxis
123
anaphylaxis
most rapid severe immediate reaction
- in minutes
124
anaphylaxis symptoms
-pruritis
-erythema
-vomiting
-diarrhea
-breathing difficulties
125
Pruritis
severe itching
126
erythma
repatches on skin
127
Delayed hypersensitive reactions
reaction occurring after several hours and are maximal several days later
128
Type I: IgE mediated
-Mediated by IgE and products of mast cells(histamine)
-most common
129
Type I initial exposure to allergen
-IgE binds to mast cell receptors
-person is considered "sensitized"
130
Type I subsequent (re-exposure) exposure
-mast cells release cytokines I = hypersensitive reaction
131
Type I affects
-Tissues with high mast cell counts
-Skin, GI, Pulmonary tract
132
Atopic
individuals predisposed to developing allergies
133
Atopic 1 parent
40% offspring will have allergies
134
Atopic 2 parents
both parents have allergies 80% children will have
135
Type II: Tissue Specific is also
Cytotoxic sensitivity
136
Cytotoxic hypersensitivity
Antibody mediated destruction of healthy host cells
137
Type II cytotoxic hypersensitivity
Immune reactions against a specific cell or tissue
138
Type II immune reactions
tissue specific antigens because they attach only on plasma membranes of certain cells
139
Type II hypersensitivity cell example
platelets- they have no antigens that can be found on any other type of cell
140
5 mechanisms of type II begins
with antibody binding to tissue-specific antigens
141
Cells are destroyed by
antibodies and complements
142
5 mechanism types
-A
-B
-C
-D
-E
143
Antibodies binding to cells
-activates complement system
-formation of membrane complex
-disintegration or rupture of cell
144
A
Cell is destroyed by antibodies and complements
145
B
Cell destruction through phagocytosis by macrophage
146
Antibodies binding to cells
macrophage recognition of cell to be phagocytized
147
C
Tissue damage caused by toxic products produced by neutrophils
148
Soluble antigens (C)
form infectious agents or hosts own cells bind to cells surface
149
Neutrophils are attracted then (C)
Release their granules into healthy cells to damage them
150
D
Antibody-dependent cell-mediated cytotoxicity (ADCC)
151
IgG antibodies bind to antigens attracting
Natural killer cells that release toxic substances that destroy cell
152
E
Target cell malfunction
-doesn't destroy cell but causes malfunction
-antibodies prevent cell interaction with normal molecules
153
Type III Hypersensitivity
Antigen-antibody immune complexes are formed in circulation and later deposited into vessel walls or extravascular tissues
154
Type IV Hypersensitivity
-No involvement of antibody/mediated T-cells
155
Type IV
-Graft rejection
-Allergic reactions from poison ivy or metals = t cell activation
=macrophage activation
= tissue damage
