Chapter 8 Flashcards
1
Q
What factors influence infection?
A
Communicability
Infectivity
Virulence
Toxigenicity
Portal of entry
2
Q
Communicability
A
Ability to spread from one individual to others and cause disease
3
Q
Infectivity
A
Pathogen ability to invade and multiply in host
-Attachment, escape of phagocytes, dissemination (spread)
4
Q
Virulence
A
Severity or harmfulness of a disease or poison
5
Q
Toxigenicity
A
Ability to produce toxins
-influences virulence
6
Q
Portal of entry
A
Route by which a pathogen infects a host
-Direct contact, inhalation, ingestion
-Animal/insect bite
7
Q
What are bacteria?
A
Prokaryotes (lack nucleus)
Aerobic or aerobic
Gram-positive or negative
8
Q
What are the 2 main factors that make gram-negative more difficult to defeat than gramp-positive?
A
Outer membrane
Porin channels
9
Q
What is a major cause of nosocomial infections?
A
Staphylococcus aureus
10
Q
Where is Staph. aureus commonly found in body?
A
Normal skin and nasal passages
11
Q
What are S. aureus virulent abilities?
A
- Produce protein that blocks compliment attack
- Avoid innate immunity by producing inhibitors that avoid recognition
- When engulfed by phagocyte, they resist lysosome by changing the chemistry of their cell walls
- Resist many antibiotics
12
Q
What are exotoxins?
A
Enzymes released from inside of pathogen
13
Q
What do exotoxins do?
A
Damage host cell plasma membrane or inactivate enzymes critical to protein synthesis
14
Q
What are endotoxins?
A
Released from outer capsule
15
Q
What do endotoxins do?
A
Activate inflammatory response and produce fever
16
Q
What systems do endotoxins activate?
A
Compliment and clotting systems
17
Q
How do endotoxins cause Hypotension?
A
They increase capillary permeability and large volumes of plasma enter surrounding tissue causing hypotension
18
Q
Bacteremia
A
Presence of bacteria
19
Q
Septicemia
A
Growth of bacteria
20
Q
Bacteremia and septicaemia are results of?
A
result of defence mechanisms failure
21
Q
What is the most common affliction of humans?
A
Viral diseases
22
Q
What does virus replication require?
A
Entry into host cell
23
Q
Describe the simple organism of a virus
A
DNA/RNA surrounded by a capsid and sometimes an envelope
24
Q
Do all viruses require medication treatment?
A
Not all, some are self-limiting
25
How are viruses transmitted?
Aerosol
Infected blood
Sexual contact
Vector (ticks, mosquitoes)
26
Cytopathic
Causing damage to living cells
27
Viruses inhibit host cell?
DNA or RNA synthesis
28
What do viruses cause the release of?
Lysosomes
-Kill host cell
29
What do viruses fuse host cell into?
Multicellular giant cell
30
What happens when a virus alters host cells antigen properties?
Immune system attacks own cells
31
How do viruses cause uninhibited growth?
Transform host cells into cancerous cells
32
What do viruses utilise to cause damage to the host?
Host cell's resources
33
Influenza
Highly contagious viral infection of respiratory passages with antigenic variation
34
Antigenic variation
Ability to change viral antigen (spikes) yearly causing dysfunction of Adaptive immune response (B/T cells)
e.g; SARS-CoV-2 virus is responsible for COVID-19
35
What are fungi?
Large eukaryotes with thick, rigid cell walls
36
What do fungal infections resist?
Penicillin
37
What ways can fungi exist?
Single-celled yeasts
Multi-cellular moulds
or both
38
How do fungi reproduce?
Simple division or budding
39
Mycoses
Diseases caused by fungi
40
Dermatophytes
Fungi that invade skin, hair or nails
41
Diseases produced by dermatophytes are called?
Tineas
e.g: Tinea capitis (scalp)
42
What do fungi adapt to?
Host environment
-Wide temperature variations, low oxygen...
43
What do fungal infections suppress?
Immune defences
44
What promotes fungal infection?
Low WBC count
45
What is the most common cause of fungal infection?
Candida albicans
46
Where is Candidia albicans found in individuals?
Normal skin microbiome
GI tract
Vagina
47
What is the most common fungal infection in cancer patients and transplantation?
Candida albicans
48
Who experiences dissemination of Candida albicans?
Immunocomprimised
-deep infection, high mortality
49
What is the death rate of disseminated candidiasis?
30-40%
50
What are parasites?
Unicellular protozoa to large worms (helminths)
e.g, flukes, nematodes, tapeworms
51
How are parasites spread?
Human to human via vectors
e.g; ticks, mosquitoes
or Ingestion of contaminated food or water
52
What is parasitic tissue damage caused by?
Toxin damage or inflammatory/immune response
53
Where does Plasmodium(malaria) occur?
In RBC
54
What occurs within 48-72 hours of having malaria?
Anemia
55
What do RBC release in malaria infection?
Cytokines
TNF-a and IL-1
56
What do the cytokines released by RBC in malaria infections cause?
Fever, chills and vommiting
57
What are antibiotics?
natural products of fungi, bacteria or other microorganisms that affect growth of specific microorganisms
58
What are the types of antimicrobials?
Bactericidal
Bacteriostatic
59
Bactericidal
Agent that kills other microorganisms
60
Bacteriostatic
Agent that inhibits growth of other microorganisms
61
What are some safeguards to infectious diseases that are poorly implemented?
-Hand hygiene
-proper sanitary disp[osal
-Water treatment
-Sanitary food transportation, prep and serving
-Control of insect vectors
-Support of research`
62
Describe the changes to antibiotic resistance over the years
1944: Penicillin effective at treating infection in British Hospital
1946: 14% of all Staphylococcus aureus penicillin resistant
1950: 59% resistant
1990: 89% resistant
63
What has caused a rise in antibiotic resistance?
Lack of compliance with therapeutic regimen
Overuse of antibiotics
64
What are vaccines?
Biological preparations of weakened (attenuated) or dead (inactivated) pathogens
65
How long does adaptive response take to activate after getting a vaccine?
2 weeks
66
what is the beneficial end result of a vaccine?
When infection by virus occurs, adaptive immunity is already prepared
-No delay
67
What is an example of a vaccine mixture?
DTap
-Diptheria, tetanus and pertussis
68
What does HERD immunity require?
85% of population immunised
69
What are toxoids?
Chemically altered pathogen toxin injected into the body so the body can learn to defeat it
70
What is passive immunotherapy?
Performed antibodies against a pathogen are given to an individual
71
Where are the antibodies used for passive immunotherapy obtained from?
Human immunoglobulin obtained from pathogen survivor
72
what is becoming the focus after a rise in antibiotic resistance?
Passive immunotherapy
73
What causes primary congenital immunodeficiency?
Genetic defect
74
What causes secondary acquired immunodeficiency?
Another illness
e.g; cancer
75
What kind of genetic defect causes primary deficiencies?
Single gene defect
76
Describe the mutations of primary deficiencies
Sporadic not inherited
Occur before birth, symptoms appear early or late in life
77
How many in Canada have primary deficiencies?
1/200
70% undiagnosed
78
How are primary deficiencies categorised into groups?
based on what aspect of immune system is defective
eg: antibody deficient
79
What are some combined deficiencies?
SCID
DiGeorge syndrome
Hypogammaglobulinemia
80
What is Severe combined immunodeficiency (SCID)?
Underdeveloped thymus causing an absence of T cells
-few detectible lymphocytes
81
What is Digeorge syndrome?
Thymus and parathyroid gland dysfunction causing inadequate T cell production and management of plasma calcium concentration
82
What is Hypogammaglobulinemia?
defect in B cell maturation or function causing lower levels of circulating immunoglobulins (antibodies) in the blood
83
What deficiencies are more common?
Secondary deficiencies
84
What is an example of a severe secondary deficiency?
AIDS, cancer
85
What is CBC (complete blood count)?
Total numbers of RBC, WBC and platelets
86
What is differential?
Individual numbers of lymphocytes, granulocytes and monocytes
87
What determines subpopulations of immunogloblins?
Quantitative determination of immunoglobulins
88
What is total complement assay?
Total number of complements in blood
89
What are some replacement therapies for immune deficiencies?
Stem cell transplants
mesenchymal stem cell injection
Gene therapy
90
Where are stem cells obtained from for stem cell transplants?
Bone marrow
Umbilical cord
-temporary improves
91
What is mesenchymal stem cell injection?
Undifferentiated stem cells found in bone marrow that undergo differentiation into other cell types.
-have potent immunosuppressive properties
92
What is gene therapy?
Insertion of normal genes into individuals genetic material to reconstitute the immune system
93
What is a potential complication associated with gene therapy?
leukaemia
94
What causes AIDS?
HIV
95
What cells are depleted in AIDS patients?
Helper T cells
96
What are Helper T cells necessary for?
Activation of both T and B cells
97
How does HIV progress to AIDS?
HIV causes dysfunctional Adaptive immune system which increases susceptibility to disease
98
AIDS most common transmission route?
heterosexual activity
99
What percent of people infected with AIDS are women?
50%
100
How can children contract AIDS from their mothers?
Via placenta, breastfeeding
101
Why is HIV vaccine difficult to develop?
It is genetically and antigenic ally variable.
Individuals have high levels of antibodies that aren't protective so if a vaccine creates antibodies they might not work
102
How is HIV treated/prevented?
Anti-retroviral therapy
103
Retroviral
Virus with RNA not DNA
104
Where are the ART sites?
Entrance inhibitors
Rever transcriptase inhibitors
Integrase inhibitors
Protease inhibitors
-Not curative, decreases death
105
Hypersensitivity
Altered immunological response to an antigen that results in disease or damage to host
106
Examples of hypersensitivity?
Allergy
Autoimmunity
Alloimmunity
107
Allergy
Harmful effects of hypersensitivity to environment (exogenous) entigens
e.g; pollen, bee sting
108
Autoimmunity
Disturbance in immunological tolerance of self-antigens (immune system doesn't recognise own antigens)
-Autoimmune diseases
109
Alloimmunity
Immune reaction to tissues of another individual
-Transfusions, transplants, fetus during pregnancy
110
What are the 4 types of hypersensitivity mechanisms?
Type I
Type II
Type III
Type IV
111
What is Type I immune mechanism?
mediated by antigen specific IgE and products of mast cells (histamine)
112
What are immediate hypersensitivity reactions?
Reaction that occurs within minutes or hours
113
Example pf immediate hypersensitivity reaction?
Anaphylaxis
-most rapid and severe
114
Anaphylaxis symptoms?
Pruritis
Erythema
Vominting, diarrhoea, breathing difficulties
115
Pruritis
Severe itching
116
Erythema
Red patches on skin
117
What is delayed hypersensitivity reactions?
reaction occurs after several hours and are at maximal days later
118
What is the most common hypersensitive reaction?
Type I
119
What are Type I against?
Environmental antigens = allergic
120
What happens when allergen is initially exposed (Type I)?
IgE binding to mast cell receptors and person become sensitised
121
What happens after a subsequent exposure to an allergen (type I)?
Mast cells release cytokines and cause a hypersensitive reaction
122
What tissues are most affected by Type I?
Tissues with more mast cells
Skin, GI tract, pulmonary tract
123
Atopic
Individuals predisposed to developing allergies
124
If one parent has allergies?
40% of offspring will
125
If both parents have allergies?
Up to 80% of offspring will
126
What is Type II hypersensitivity?
Tissue specific or cytotoxic
-Antibody mediated destruction of healthy host cells (specific cell or tissue)
127
What are tissue-specific antigens?
Attach only to plasma membranes of certain cells
e.g; platelets have antigens found on no other cell in body
128
What are the 5 mechanism of Type II?
A, B, C, D, E
129
What does each Type II mechanism begin with?
Antibody binding to tissue-specific antigens
130
Type II A mechanism?
Cell is destroyed by antibodies and complements (Membrane attack complex)
131
Type II B mechanism?
Cell destruction through phagocytosis by macrophage
132
Type II C mechanism?
tissue damage caused by toxic products produced by neutrophils
Soluble antigens from infectious agents or host’s own cells bind to cell surface.
Neutrophils are attracted and release their granules into healthy cells= damage cells
133
Type II D mechanism?
Antibody- dependent cell mediated cytotoxicity (ADCC)
-Binding of IgG antibodies attracts NK cells that release toxins to destroy cell
134
Type II E mechanism?
Target cell malfunction (not destruction) because antibody prevents cells from interacting with normal molecule
e.g; Grave's disease targets thyroid
135
What is Type III hypersensitivity?
Immune complex
- ˜antigen–antibody immune complexes are formed in circulation and later deposited in vessel walls or extravascular tissues
136
What is Type IV hypersensitivity?
Cell mediated (T cells activated--> macrophages --> cell destroyed)
-NO ANTIBODIES
Example: graft rejection, allergy to poison ivy, metals
