Chapter 8- Infection and Defects in Mechanisms of Defense Flashcards

1
Q

the ability to spread from one individual to others and cause disease

A

communicability

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2
Q

this is the severity or harmfulness of a disease or poison

A

virulence

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3
Q

pathogen ability to invade and multiply in host

A

infectivity

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4
Q

ability to produce toxins – greatly influence pathogen’s virulence

A

toxigenicity

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5
Q

route by which a pathogen infects host. E.g., direct contact, inhalation or ingestion; bites of an animal or insect

A

portal of entry

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6
Q

two factors that make gram - more difficult to defeat than gram +

A

outer membrane and porin channels

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7
Q

this bacteria is life threatening, common on normal skin and nasal passages and major cause of nosocomial infections

A

staphylococcus aureus

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8
Q

staphylococcus aureus resists actions of many ______

A

antibiotics

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9
Q

what are the two types of toxins production?

A

endotoxins & exotoxins

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10
Q

which toxin production is released from the inside and enzymes that damage host cell plama membrans or inactive enzymes critical to protein synthesis

A

exotoxins

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11
Q

which toxin production is released from outer capsul and activate inflammatory response and produce fever

A

endotoxins

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12
Q

what are the result of defense mechanisms failure

A

bacteremia (presense) & septicemia (growth)

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13
Q

what does endotoxin do in our body?

A

activate inflammatory response and activate complement and clotting systems, which leads to increased capillary permeabilty, large volumes of plasma into surrounding tissue and resulting in hypotension

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14
Q

what disease is most common affliction of humans, replication requires entry into host cell and self-limiting

A

viral disease

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15
Q

in viral disease, DNA/RNA surrounded by ____ and perhaps envelope

A

capsid

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16
Q

what are the ways people transmit viral disease

A

aerosol, infected blood, sexual contact and vector

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17
Q

what is cytopathic

A

causing damage to living cells

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18
Q

this is a type of viral disease that is highly contagious viral infection of respiratory passages

A

influenza

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19
Q

the ability to change viral antigen yearly

A

antigenic variation

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20
Q

what is responsible for COVID- 19

A

SARS-CoV-2 virus

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21
Q

what does antigen utilize to active in order carry out antigenic variation

A

adaptive immune response

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22
Q

in order to change antigen, _____ adaptive immune response must occur

A

dysfunction

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23
Q

what infection resist penicillin, as wells as these are large eukaryotes with thick and rigid cell walls

A

fungal infection

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24
Q

fungal infection exist as single- celled ____, multi-cellular ____ or both

A

yeasts; molds

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25
what is the reproduction of fungal infection: simple ____ or _____
division; budding
26
what are mycoses
diseases caused by fungi
27
what are dermatophytes
fungi that invade skin, hair or nails
28
what do you call to the disease dermatophytes produce
tineas
29
pathogenicity is when the fungus adapt to the host environment due to ____ temperature variation and ____ O2
wide; low
30
low ___ blood cell count promotes fungal infection
white
31
this is the most common fungal infection
candida albicans
32
where does candida albicans found most likely?
normal skin microbiome, GI tract and vagina
33
in candida albicans, most common fungal infections are in ____ patients and transplantations
cancer
34
death rate of disseminated candidiasis is ____
30%-40%
35
this infection is spread to human to human via vectors (e.g., ticks and mosquitos) or ingestion of contaminated food or water
parasitic infection
36
parasitic infection are ____ protozoa to large worms
unicellular
37
Plasmodium (malaria) occurs in ____ blood cells
red
38
what countermeasures are natural products of fungi, bacteria or other microorganisms that affect growth of specific microorganisms
antibiotics
39
two types of antimicrobials
bactericidal & bacteriostatic
40
what antimicrobial kills other microorganisms
bactericidal
41
what antimicrobial inhibits growth of other microorganisms
bacteriostatic
42
what caused the rise in antibiotic resistance?
lack of compliance with therapeutic regimen: not using antibiotic for prescribed duration. As a result, strongest microbes are left alive = repopulation with pathogens resistant to specific antibiotic
43
what consequence is the destruction of normal microbiome
overuse of antibiotics
44
what % of HERD immunity usually requires
85%
45
this countermeasures is the biological preparations of weakened (attenuated) or dead (inactivated) pathogen
vaccines
46
adaptive response of vaccine is usually require ___ weeks to activate
two
47
what is the vaccine mixture?
DTaP vaccine -- diptheria, tetanus and pertussis (aka whooping cough)
48
what countermeasures is when chemically altered pathogen toxin is injected into body
toxoids
49
this countermeasure preformed antibodies are given to individual
passive immunotheraphy
50
passive immunotherapy becomes the focus after the rise of antibiotic ____
resistance
51
what are the 2 deficiencies in immunity
primary & secondary
52
what is primary deficiencies
aka congenital; caused by genetic defect
53
what is secondary deficiency
aka acquired; caused by another illness
54
primary deficiency is most result of a ____ gene defect
single
55
in primary deficiency, mutation occurs ____ birth but ____ may appear early or late in life
before; symtoms
56
in Canada, __ in 200 have primary deficiency
1
57
primary deficiencies are categorized in ___ based upon what aspect of immune system is defective
groups
58
some combines deficiences are?
SCID, DiGeorge syndrome and Hypogammaglobulinemia
59
what combined deficiency is underdeveloped thymus?
SCID
60
when there is underdeveloped thymus there is absence of ____ cells
t-cells
61
which combined deficiency acquired when thymus and parathyroid dsyfunctions
DiGeorge syndrome
62
when a person have DiGeorge syndrome, they have inadequate ___ cell production and management of plasma __
t; calcium
63
what is the result of hypogammaglobulinemia
defect in B cell maturation or function
64
in hypogammaglobulinemia, there are lower levels of circulating ______ in blood
immunoglobulins or antibodies
65
secondary deficiencies are ___ common than ____ deficiency but not at ____ relevant
far; primary; clinically
66
AIDS/ Cancer are extremely ____ secondary deficiencies
severe
67
what is complete blood count or CBC
the total numbers of RBC, WBC and platelets
68
what is differential in terms of evaluation of immunity?
individual numbers of lymphocytes, granulocytes and monocytes
69
what is total complement assay
total # of complements in blood
70
____ determination of immunoglobulins which determines ___ of immunoglobulins
quantitative; subpopulations
71
Stem cell transplantation from ___ ____, _____ cord cells
bone marrow; umbilical
72
what result of reconstitution of immune system
gene therapy
73
what is some caution of gene therapy
some reciepients develop leukemia
74
what is gene therapy
inserted normal genes into their genetic material
75
what is mesenchymal stem cell (MSCs) injection
undifferentiated stem cells found in bone marrow which undergo differentiation in other cell types
76
which replacement therapies have potent immunosuppressive properties
mesenchymal stem cell
77
what syndrome caused by viral disease
HIV
78
what are the result of HIV
dysfunctional adaptive immune system; increased susceptibility to disease and AIDS
79
when the person has HIV, it depletes ____ ___ cells
helper t
80
helper t cells are necessary for activation of both __ and ___ cells
t; b
81
_____ activity is most common transmission of AIDS
heterosexual
82
women constitute more than ___ % of people infected of AIDS
50%
83
what are some difficulties with vaccine development with HIV?
people with HIV have high levels of antibodies but don't appear to be protective; HIV genetically and antigenically variable
84
what is epidemiology
branch of medicine that deals with incidence, distribution and possible control of diseases
85
what is the treatment and prevention of HIV
ART or anti-retroviral therapy
86
retroviral means virus with ___ not DNA
RNA
87
ART is a combination of following effects?
entrance inhibitors, reverse transcriptase inhibitors, integrase inhibitors and protease inhibitors
88
what is hypersensitivity?
altered immunological response to an antigen that results in disease or damage to host
89
this type of hypersensitivity is due to harmful effects of hypersentivity to environmental antigen
allergy
90
this hypersensitivity is a disturbance in immunological tolerance of self-antigens
autoimmunity
91
this hypersensitivity is due to immune rxn to tissues of another individuals -- observed from transfusions, transplants or fetus during pregnancy
alloimmunity
92
what are the mechanisms of hypersensitivity?
type I - IgE mediated type II - tissue specific rxn type III - immune complex mediated type IV - cell mediated
93
most hypersensitive rxns include ___ than one type
more
94
reactions that occurs within minutes or hours?
immediate hypersensitive rxns
95
most rapid and severe immediate rxns -- within minutes
anaphylaxis
96
symptoms of anaphylaxis?
pruritis - sever itching erythema - red patches on skin vomiting, diarrhea and breathing difficulties
97
reaction occurs after several hours and are at maximal several days later
delayed hypersensitivity rxns
98
what is the product of type I hypersensitivity
mast cells, primarily histamine
99
which is the most common hypersensitive rxns
type1
100
what is term called for individuals predisposed to developing allergies?
atopic
101
if one parent has allegies, what & of offspring will have allergies?
40%
102
if both parents have allergies, what % of the child will have allergies?
80%
103
type I is against ____ antigens, therofore ___
environmental; allergic
104
mast cells release of ____ which leads to hypersensitive rxn
cytokines
105
tissues with high mast cells are most commonly affected of type I such as?
skin, GI tract and pulmonary tract
106
type II hypersensitivity is also called as?
cytotoxic hypersensitivity
107
what does type II (aka cytotoxic hypersensitivity does to the body?)
antibody mediation destruction of health host
108
which type of hypersensitivity have immune rxns against a specific cell or tissue
type II: tissue mediated
109
why type II hypersensitivty called tissue-specific antigens?
they attach only on plasma membranes of certain cells
110
what are the five mechanisms of type II?
A - cell is destroyed by antibodies and complements B - cell destruction through phagocytosis by macrophage C- tissue damage caused by toxic products produced by neutrophils D - antibody- dependent cell mediated cytotoxicity (ADCC) E - target cell malfunction. E.g., grave's disease - targets thyroid.
111
what happens when antibody binding to cell in mechanism A?
- activation of complement system - formation of membrane attack complex - disintegration or rupture of cell wall.
112
the binding of ____ antibodies to antigens is what mechanisms?
IgG; mechanism D
113
what attracts the binding of IgG antibodies?
natural killer cells
114
antibody prevents cells interaction with _____ malfunction
normal
115
what is the type III hypersenstivity called?
immune complex
116
how was antigen-antibody immune complexes formed?
in circulation
117
where was immune complex deposited?
in vessel walls or extravascular tissues
118
what is type IV hypersensitivity?
cell mediated
119
does not involve _____, and mediated by ____ cells
antibody; t
120