8. Infection and Defects in Mechanisms of Defense Flashcards
1
Q
ability to spread from one individual to others and cause disease
A
communicability
2
Q
ability of a pathogen to invade and multiply in the host
A
infectivity
3
Q
capacity of a pathogen to cause severe disease
A
virulence
4
Q
ability of an agent to produce disease
A
pathogenicity
5
Q
What does pathogenicity of an agent depend on?
A
their communicability, infectivity, extent of tissue damage, and virulence
6
Q
route to infect a host
A
portal of entry
7
Q
ability to produce soluble toxins or endotoxins (greater influence pathogen’s degree of virulence)
A
toxigenicity
8
Q
opportunistic bacteria that is commonly found on skin and nasal passages but is also a major cause of HAI and abx resistance
A
staphylococcus aureus
9
Q
thick capsule that helps microbes adhere to plastic/prosthetics
A
biofilm
10
Q
T/F: S. aureus uses biofilms to colonize but doesn’t produce toxins
A
False: produces and secretes exotoxins as well as uses biofilms
11
Q
proteins created and secreted by the bacteria to have a virulence effect -> can damage plasma membranes or inactivate enzymes needed for protein synthesis
A
exotoxins
12
Q
Explain how endotoxins can activate inflammatory response and produce fever
A
When bacterial cell dies -> membrane is disrupted -> releases LPS (lipid A portion) -> lipid A exposed to the immune system -> causes fever, shock, and DIC
13
Q
what type of bacteria produce endotoxins?
A
gram-negative bacteria
14
Q
Explain what causes endotoxic shock
A
bacteria growing in blood (septicemia) -> release endotoxins -> activate complement and clotting systems -> increased capillary permeability -> large volumes of plasma escape to surrounding tissues -> hypotension -> shock
15
Q
4 ways of transmitted viruses
A
- aerosol - infected blood - sexual contact - vector (ex. mosquitos)
16
Q
changing of viral surface antigens to evade the immune system (seen in influenza)
A
antigenic variation
17
Q
antigenic drift vs shift
A
- antigenic drift: minor change in surface antigens due to mutations -> leads to weakened protection against virus - antigenic shift: major change where genome is segmented and undergoes recombination (usually zoonotic)
18
Q
What 2 proteins classify influenza and what do they do?
A
- H protein (hemagglutinin): attachment and fusion (entry into cell) - N protein (neuraminidase): facilitates release of viral proteins from host cell
19
Q
large microorganisms w/ thick, rigid cell walls without peptidoglycan
A
fungus/mycoses
20
Q
Because fungus cell wall is missing peptidoglycans, what medications are they resistant to?
A
penicillins and cephalosporins
21
Q
- most common cause of fungal infections - opportunistic fungus that is normally found in the skin, GI tract, and vagina but can cause localized infection if overgrown -> disseminates if immunocompromised
A
Candida albicans
22
Q
eukaryotic, unicellular microorganisms include malaria, amoeba, and flagellates
A
protozoa
23
Q
how do protozoa spread?
A
via vectors or ingestion
24
Q
Bactericidal vs Bacteriostatic
A
- bactericidal: kill bacteria; # of cells in the colony will decline after administration of abx - bacteriostatic: arrest growth -> stops cells from doubling and allows host immune system to take care of them
25
What causes antibiotic resistance?
- genetic mutations - lack of compliance (selective resurgence) - overuse (destruction of normal microbiome)
26
live viruses that are weakened
attenuated
27
Who should not receive live attenuated vaccines?
individuals w/ deficient or suppressed immune systems -\> may cause life-threatening infection
28
purified exotoxins that have been chemically detoxified without the loss of immunogenicity (used in vaccines)
toxoids
29
countermeasure against pathogens where preformed antibodies are given to individuals
passive immunotherapy
30
Lab/serum tests used to evaluate immunodeficiencies
- CBC w/ diff - quantitative determination of immunoglobulins - assay for total complement
31
Name 6 types of treatments for immunodeficiencies
- gamma-globulin therapy (IVIg) - stem cell transplantation - transfusion of erythrocytes - BM transplants - mesenchymal stem cell injection - gene therapy
32
What type of immunity are vaccines?
active artificial
33
What do bacteria produce to destroy penicillin and become resistant to it?
B-lactamase
34
List the 6 stages of viral infection of a host cell
- attachment - penetration - uncoating - replication - assembly - release
35
What do all viruses contain?
genome and capsid
36
MOA of most antibiotics (4)
- inhibition of function/production of cell wall/membrane - prevent protein synthesis - blockage of DNA replication - interference w/ folic acid metabolism
37
primary vs secondary immune deficiencies
- primary: congenital - secondary: acquired
38
3 most common primary immune deficiencies
- common variable immune deficiency - selective IgA deficiency - IgG subclass deficiency
39
deficiencies that result from defects that affect development of both B and T cells
combined deficiencies
40
group of AD and X-linked disorders where T cell function is always impaired and function will vary with B cells
severe combined immunodeficiencies (SCID)
41
immune deficiency characterized by inability of lymphocytes and macrophages to produce HLA I or HLA II
bare lymphocyte syndrome
42
x-linked disorder where IgM production is greatly depressed
Wiskott-Aldrich Syndrome
43
clinical triad of wiskott-aldrich syndrome
eczema, thombocytopenia, and immune deficiency
44
congenital mutation that causes thymic hypoplasia or aplasia, hypoparathyroidism, congenital heart defects, and characteristic facial features
DiGeorge syndrome
45
What do each of the following mutations in DiGeorge syndrome lead to? - thymic hypoplasia/aplasia - hypoparathyroidism
- thymic hypoplasia/aplasia: decreased number of T cells and T cell function - hypoparathyroidism: low blood calcium levels -\> develop tetany
46
What facial features are seen in DiGeorge syndrome?
low ears and wide eyes
47
What complications are seen from selective IgA deficiency
recurrent sinus infections, respiratory infections, and stronger environmental allergies
48
caused by a mutation in the pathway for B cell development but pt will have normally developed T cells
Bruton's syndrome (X-linked agammaglobulinemia)
49
What types of infections will be seen in Bruton's syndrome?
recurrent upper and lower respiratory infections w/ encapsulated bacteria
50
mutation in NADPH oxidase -\> phagocytes take up Ags but can't destroy them -\> chronically infected
chronic granulomatous disease (CGD)
51
What happens in patients with C3 deficiency?
loss of C3 (central to complement pathway) -\> inability to activate C5 -\> recurrent life-threatening infections soon after birth
52
What cells are destroyed by HIV? What is the purpose of these cells?
CD4 Th cells -\> necessary for development of plasma cells and CD8 cytotoxic T cells
53
How is HIV spread?
blood-borne and sexual contact (more common)
54
viruses that carry genetic material in the form of RNA rather than DNA
retroviruses
55
What do retroviruses use to implant their ds DNA into host cells?
- reverse transcriptase: RNA -\> DNA - HIV integrase: inserts DNA into host genes
56
essential enzyme in processing proteins needed from the viral internal structure (capsid)
protease
57
Describe the general steps of HIV life cycle (6)
- virion binds to CD4 and chemokine receptor - fusion of membrane w/ host cell membrane -\> genome enters cytoplasm - reverse transcriptase -\> integration of virus genes into host genome - transcription of HIV genome into RNA - synthesis of proteins and assembly of virion core - budding and release of mature vision
58
List 4 types of medication MOAs that treat/prevent AIDS
- HIV fusion inhibitors (prevents entrance into host cell) - reverse transcriptase inhibitors - HIV protease inhibitors - HIV integrase inhibitors
59
current regimen for treatment of HIV (combination of drugs)
antiretroviral therapy (ART)
60
Name 2 lab tests use to determine the progression of HIV
- HIV RNA levels: determines viral load - CD4 T cell count
61
Normal CD4 T cell count and value that begins to cause opportunistic infections
- Normal: 800-1000 - Opportunistic infections: \< 200
62
Describe typical HIV progression without treatment
- exposure: viral load is high (first 6-12 weeks) - clinical latency: viral load is low (no sxs) but it could still be transmitted (12 weeks - 7 years); CD4 count drops slowly over time - Constitutional sxs as viral load begins increasing - Opportunistic diseases occur as CD4 \< 200
63
Clinical symptoms of AIDS
- cachexia (severe weight loss) - Kaposi sarcoma - PCP pneumonia - other atypical or opportunistic infections or cancers
64
How can HIV be transmitted to infants?
during pregnancy, at delivery, or through breastfeeding
65
Which system is typically involved in pediatric AIDS?
neurologic involvement -\> HIV encephalopathy
66
altered immunologic response to an antigen that results in disease or damage to the host
hypersensitivity
67
deleterious effects of hypersensitivity to environmental (exogenous) antigens
allergy
68
disturbance in the immunologic tolerance of self-antigens
autoimmunity
69
immune reaction to tissues of another individual
alloimmunity
70
Hypersensitivity I, II, III are mediated by what? How does this differ from hypersensitivity IV?
- mediated by Abs - Type IV is cell mediated
71
type I hypersensitivity is mediated by what?
IgE mediated against environmental antigens (allergens)
72
sensitizing exposure and re-exposure in type I hypersensitivity
- sensitizing exposure: allergen binds to APC -\> B cell + Th2 cell -\> plasma cell -\> creates IgE -\> binds to IgE Fc receptor on mast cell - re-exposure: allergen enters -\> binds to IgE on mast cells -\> mast cell degranulation -\> histamine release -\> edema/smooth muscle contraction/mucous secretion
73
Symptoms of type I hypersensitivity
- itching/urticaria - angioedema - hypotension - bronchospasm (anaphylaxis) - dysrhythmia
74
type II hypersensitivity is mediated by what?
specific cell or tissue (tissue-specific antigens)
75
5 mechanisms of type II hypersensitivity
- cell is destroyed by abs and compliment - cell destruction through phagocytosis - soluble antigen may enter circulation and deposit on tissues -\> destroyed by complement and neutrophils - Ab dependent cell mediated cytotoxicity (ADCC) - target cell malfunction
76
Ex. of type II hypersensitivity
- Graves disease (hyperthyroidism) - myasthenia gravis - Hemolytic disease of newborn (HDNB)
77
type III hypersensitivity is mediated by what?
immune complex mediated (not organ specific) -\> antigen-antibody complex circulate and later deposited in vessel walls or extravascular tissues
78
Ex. of type III hypersensitivity
- serum sickness (includes Raynaud phenomena) - arthus reaction - SLE
79
type IV hypersensitivity is mediated by what?
cell-mediated; either cytotoxic T lymphocytes or lymphokine-producing Th1 and Th17 cells -\> direct killing of target cells
80
Ex. of type IV hypersensitivity
- graft rejection - TB skin test - contact dermatitis (poison ivy, metals, and latex)
81
T/F: individuals w/ allergies are typically genetically predisposed to them
True
82
may reduce severity of allergic reaction but could also cause anaphylaxis
desensitization
83
breakdown of tolerance to where the body recognizes self-antigens as foreign
autoimmunity
84
autoimmune disease characterized by production of a large variety of antibodies (autoantibodies)
systemic lupus erythematosus (SLE)
85
Explain how SLE is a type III hypersensitivity
causes deposition of circulating immune complexes containing antibody against host DNA
86
List some of the clinical manifestations of SLE
- arthritis/arthralgia - vasculitis/rash - renal disease - hematologic changes - CV disease
87
How is SLE diagnosed?
presence of 4 or more: - facial rash - discoid rash (raised patches w/ scaling) - photosensitivity - oral/nasal lesions - arthritis of at least 2 peripheral joints - pleurisy/pericarditis - renal, neuro, or hematologic disorders - presence of ANA (antinuclear antibodies) in blood
88
Where are Rh antigens expressed?
only on RBCs
89
3 types of transplant rejection
- hyperacute: due to preexisting ab to the antigens of the graft - acute: cell-mediated immune response (type IV) against unmatched HLA antigens - chronic: takes months-years; weak cell-mediated reaction against minor HLA antigens
