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155 Cards in this Set

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Pathogens that survive by characteristic virulence factors that allow evasion of phagocytic cells
extracellular pathogens
pathogens with virulence factors that allow for survival in phagocytic cells
Intracellular pathogens
Term for pathogens that can infect a healthy host
primary pathogens
Infection of an already diseased host
opportunistic infection
Term for number of organisms required to establish infection of average
infectious dose
microbial chemical factors required for establishing disease
virulence factors
Name the two common virulence factors
1. endotoxins (released when microbe is damaged
2. exotoxins (secreted from microbe)
When toxins are spread via the blood stream
enzymes that degrade connective tissues of our cells, allowing spread of microbes
toxins or enzymes that cause RBCs to lyse
hemolysing toxins
disease in which s/s of disease are visible
clinical disease
walled off, discrete infections to which immune cells can't gain access
bacteria in the blood
actively growing bacteria in the blood; life threatening
viruses in the blood
specific problems following a disease; i.e. paralysis following polio
4 common viral latency diseases
herpes, hep b, HIV, and Epstien Barr
host who shed microbes during latent stage; can spread disease during latency
chronic carrier
decreased WBCs
Increased WBCs
The study/identification of new diseases and how they spread
an inanimate object capable of carrying infectious organisms
Factors of gram + cells that allow different microbes to attach to target cells
Fimbrae and lipoteichoic acid
Endotoxin found in gram - bacterial lipid A
An exoenzyme that functions to destroy host connective tissue, which facilitates bacterial spreading
Cells that sweep mucous layers toward bodily orifices
ciliated epithelial cells
An enzyme found in bodily secretions that degrades bacterial cell walls
Protein found in bodily secretions that sequesters iron to prevent availability to microbes
iron binding proteins
Small proteins released by infected macrophages, fibroblasts, and T cells that alert neighboring cells which then defend themselves
A special set of proteins that activate through the body and bind to bacteria
Refers to sequential order of compliments
compliment cascades
List the 3 steps classical pathway of compliment system
1. C1 binds to bacterial bound Abs and becomes activated and causes binding of activation of C4,C2, C3, and C5 in that order

2. Pieces of C3 and C5, C3a and C5aare cleaved free of bacteria and act as chemotactic facts; increase vascular permeability to allow phagocytes better access

3. C3b and C5b (b for binding) serve as focal point for compliment components C6, C7, C8, and C9 to bind as complex cells
the phagocytes process of exiting the blood stream and squeezing between vascular endothelial cells
Forms pore through bacterial membrane so that leakage, lysis and death of microbe result
membrane attack complex
pathway that starts with C3 and binds directly to certain microbial polysaccharides; prevents infections before Ab production has time to occur d/t compliment proteins being always present in blood
Alternate compliment pathway
What is the significance of C3 deficiency?
Increased bacterial infection because both the classical and alternate compliment pathways require C3 to function
Another name for C3b, literally means "to prepare to eat"
contains specific receptor for phagoctic polymrphanuclear leukocytes (PMNs)
Another name for PMNs; nuclei stains with neutral dye
primary type of phagocytic cell, makes up 55% of all WBCs with large reserve in bone marrow for acute infections
How long do neutrophils live?
1-5 days
Cells that make up 8% of WBCs, called monocytes in blood, alveolar macrophages in lungs, kupffer cells in liver and dendritic cells in skin
How long can macrophages live?
months to years at tissue site, 0 backup in bone marrow
Cells that signal other cells; one type is secreted by monocytes
4 steps of phagocytosis
1. phagocytes recognize C3a and C5a near site of infection and adhere to blood vessel walls near it
2. use diapedesis to squeeze between the cells that form the vessel walls
3. migrate by ameoboid movement toward highest concentration of C3a and C5a cells
4. ingest particles into phagsosome which then fuse to lysosomes
Conditions that inhibit phagocytes
1. poorly oxygenated tissues i.e. necrotic tissue/tissues of diabetics
2. low pH (most bacteria produce acid)
3. fluid filled spaces i.e spinal column (inhibits motility)
The two principle nonphagocytic cells of natural immunity
1. basophils
2. eosinophils
Cells that release histamine and related chemicals causing inflammation and attracting phagocytes; similar to mast cells
Cells that release toxins important in overcoming infections by worms and other parasites too large for phagocytes to ingest
Part of both basophils and eosinophils that contain histamine and various toxic chemicals
What do PMNs and macrophages both have receptors for?
IgG Abs and C3b
List seven natural physical barriers to infection
skin, mucus, ciliated epithelial cells, fluid flow, acidity i GI tract, urea and interferons
Any substance that causes the immune system to produce antibodies against it; usually proteins or polysaccharides
antigens (Ags)
A localized region on the surface of an antigen that is capable of eliciting an immune response and of combining with a specific antibody to counter that response.
a protein molecule of the immune system that binds with Ags
antibody (Ab)
A substance that is capable of reacting with a specific antibody but cannot induce the formation of antibodies unless bound to a carrier protein or other molecule; fit into Ab binding sites
Our own Ags
foreign ags
non self
Occurs when new immune cells recognize self ags (they fail to mature and die)
The three hallmarks of acquired immunity
1. Inducibility
2. Specificity
3. Memory
Hallmark of acquired immunity involving contact c foreign material that stimulates immunity
Hallmark of acquired immunity in which resultant immunity following inducibility recognizes only the stimulatory agent
Hallmark of acquired immunity in which subsequent exposure results in faster and greater response to identical foreign material
A subset of leukocytes responsible for acquired immunity by specifically recognizing foreign Ags; originate in bone marrow.
Lymphocyte that leaves the bone marrow and travels to thymus for maturation
T Lymphocyte aka T cell
Lymphocyte that gets its name because it matures in bone marrow; Ab producing cells.
B lymphocyte aka B cell
What causes B cell proliferation?
When it comes into contact with a specific Ag that binds to its surface Ab.
Daughter cells of B cells that secrete Abs of the same type that originally bound to the Ag; survive for weeks to months.
plasma cells
Daughter cells of the B cells that remain essentially identical to the first B cell; last for many years; memory of the acquired immune response.
memory cells
How long does it typically take for B cell proliferation to result in ample Ab production?
7-10 days
Specific surface receptors of T cells that recognize foreign Ags
T cell receptor
Subset of t cell that recognize specific Ags and cause proliferation of other immune cells
T helper (Th) cells
Daughter cells of B cells that secrete Abs of the same type that originally bound to the Ag; survive for weeks to months.
plasma cells
Daughter cells of the B cells that remain essentially identical to the first B cell; last for many years; memory of the acquired immune response.
memory cells
How long does it typically take for B cell proliferation to result in ample Ab production?
7-10 days
Specific surface receptors of T cells that recognize foreign Ags
T cell receptor
Subset of t cell that recognize specific Ags and cause proliferation of other immune cells
T helper (Th) cells
Protein expressed on Th cell surfaces that is a marker used to id the cells
Protein produced on the surfaces of T cells that are called T suppressors (Ts) or cytotoxic T (Tc) cells
Deletion of B and T cells that recognize self Ags; occurs early in a person's life
clonal deletion
A cell, originating in the bone marrow and subsequently found as a dendritic cell in various locations, that facilitates the immune response by holding antigens on its surface and presenting them to lymphocytes.
antigen-presenting cell
Three cells required for B and T cells to proliferate and make memory cells
1. Th cell
2. APC
3. a third lymphocyte (can be b or t cell)
A subset of cytokines that are made by leukocytes
Interleukin produced by the APC that stimulates the Th cell to bind to the presented Ag fragment
interleukin 1 (IL1)
Interleukin secreted by a Th cell once it recognizes the Ag produced by the APC and is stimulated by IL1
interleukin 2 (IL2)
Term for the stimulating Ag
Response seen when protein is the Ag; Ab secreting plasma cells and memory B cells are both formed
T-dependent response
Usually seen in polysaccharide Ags; only plasma cells are produced; short term immunity as no memory cells are produced
T-independent response
The end of an Ab molecule with only the heavy protein chains; the stem of the Y
Fc region
The upper fragments of the Ab molecule; contain actual binding sites
fragment antigen binding (Fab)
The name for the binding ends of the Fab; so called because of the highly variable amino acid sequences
variable region
The rest of the chains including the lower two thirds of the Fab region are called the ____________ regions
constant regions
Draw and label an Ab molecule
Ab molecule:
What allows Abs to cross link Ags into larger complexes that are more easily destroyed by the immune system?
The two identical binding sites found on each Ab molecule
the name given to Ab proteins that have been isolated from the blood
immunoglobulin (Ig)
How many structual classes of Ab molecules are there?
Term for globular or roundish protein
Characteristics: most abundant Ab class in blood; longest half-life (21 days); crosses placenta;protective for first 3-6 mos of life
Binding sites: 2
Characteristics: found on surface of B cells (Ag receptor)
Binding sites: 2
Characteristics: very little found in blood; bound to basophils and mast cells
Binding sites: 2
Characteristics: most abundant Ig in body; two Ys linked at Fc end by J-chain +secretory piece
Binding sites: 2 in blood, 4 in secretions
Characteristics: J chain, a single Y version is also found on the surface of B cells; mostly degraded after 4 weeks
Binding sites: 10
The first class of Ab to appear when foreign Ag stimulates immune response; only one to appear in case of T-independent Ags
List the order of Ab class appearance in T-dependent responces
IgM, IgG, IgA, IgE
The process by which bacteria are altered by opsonins so as to become more readily and more efficiently engulfed by phagocytes; IgG
Coming from one clone or cell
The binding of compliment proteins; usually initiated by AgG or IgM binding to an Ag; can be used to quantify antigens in a lab
compliment fixation
The formation of large aggregates of microbes
A convenience lab tool used to id the formation of smaller aggregates with Abs
Assay in which radioactive chemicals are added to Ab molecules and then centrifuged to quantify number of bacteria
Assay similar to Radioimmunoassays except florescence chemical is used instead of radioactive chemicals; quantified c UV light
Fluorescent Ab Assay
An assay that binds an enzyme to an Ab molecule that breaks down one selected chemical into two, one of which is colored
Enzyme Linked Immunosorbent Assay (ELISA)
When Abs are used to inactivate viruses
neutralization reactions
Test in which viral proteins are spread out on polyacrylamide gel by means of electric current to separate each protein; separated proteins are transferred to special filter paper which is treated c pts serum; highly accurate.
Western Blot Analysis
Immunization in which host's immune system is induced by attenuated microbes; life long immunity
active immunization aka active vaccination
The general process of increasing a specific type of the body's immune capability to a living or inanimate Ag
The stimulation of an immune response that protects against a specific infectious agent that lives
A type of immunization but not vaccination when we transfer specific Abs fro one individual to another
passive immunization
Diseases in which the number of viruses reaches huge numbers and end up being filtered out by the kidney; this leads to glomerulonephiritis, arthritis, and vasculitis.
immune complex diseases
An immune complex disease resulting from a reaction to proteins in antiserum derived from a non-human animal source
serum sickness
antigens that induce allergies
Term for people with high levels of IgE resultant allergies; first exposure produces IgM, subsequent exposures stimulate IgE; activates mast cells and basophils
A cellular process that releases antimicrobial cytotoxic molecules from secretory vesicles called granules found inside some cells
A type of allergic reaction in which there is a local skin lesion that is red, raised and watery
weal and flare
A type of shock that can occur when histamine is release systemically; B/P drops precipitously and death can occur in minutes
anaphylactic shock
The early exposures that lead to IgE binding to cells resulting in sensitivity to the Allergen
Abs stay in the fluid; essentially Ab-mediated immunity
humoral immunity
Immunity conferred by WBCs, especially T cells
cell-mediated immunity
Surface proteins that recognize or are recognized by other cells
Receptors of cell mediated immunity; present in two forms
major histocompatibility complex (MHC)
Form of MHC found on all cells except RBCs
Class I aka MHC-I
Form of MHC found primarily on macrophages and B cells
Class II aka MHC-II
How does cell mediated immunity work
See leukocyte stimulation
The function of Th cells in cell mediated immunity
induce immune response
The function of Tc cells in cell mediated immunity
destroy infected host cells
A toxic protein secreted by Tc cells that opens channels in infected cells and kills them to cause d/c of production on microbes
What causes raised hardened area of positive PPD test?
Tc cells
The key cell in causing delayed type hypersensitivity (DTH)
Tc cells
Cause: IgE molecules bound to basophils and mast cells bind allergens causing release of histamine and other chemicals
Examples: Hay fever, asthma
-Occurs immediately
Type I Immunological Hypersensitivity reaction
aka IgE mediated hypersensitivity
aka anaphylactic hypersensitivity
aka immediate hypersensitivity
Cause: IgM or IgG Abs bind to Ags on the body's own cell
Examples: hemolitic disease of newborn (HDN), blood transfusion rejection
Type II reaction
aka cytoxic or cytoltic hpersensitivity
Passive immunization given to preg women to prevent HDN
naturally occurring Abs; An isoantibody normally present in the serum of an individual that causes the agglutination of the red blood cells of another individual of the same species.
Cause: formation of small complexes of Ag and Ab
Type III reaction
immunocomplex diseases
Cause: No Abs are involved; destruction is d/t Tc cells
-requires one to two days to develop
Type IV reaction
aka cell-mediated immunity reaction
aka delayed hypersensitivity
Immunodeficiency disease in which pts make no Ab
TX: periodic injection of pooled human gamma globulins
Bruton's disease
Immunodeficiency disease in which the thymus fails to develop resulting in T-independent responses only
TX: bone marrow transplant
DiGeorges Syndrome
Immunodeficiency disease in which stem cells in bone marrow are defective and do not produce B or T cells
TX: bone marrow transplant
Severe combined immunodeficiency
Diseases in which the immune system mistakenly recognizes self Ags and attacks them
Autoimmune diseases
Autoimmune disease in which the pts IgM recognizes their own IgG and produce immune complexes that are deposited in joints and kidneys where damaging inflammation occurs.
Rheumatoid arthritis
Autoimmune disease in which Abs destroy the insulin producing cells of the pancreas
Insulin dependent DM
Autoimmune disease in which Abs destroy nucleic acid material from pt's cells, results in in immune complex disease
Systemic lupus erythematosus
Autoimmune disease in which T cells destroy the sheath that covers neurons; results in paralysis
Autoimmune disease in which Abs react with nerve cell receptors to interrupt neuronal signaling
Myasthenia gravis
Which Ab classes opsonize Ags?
IgG, IgM
How do Abs fix compliments?
IgG, IgM; when both bind to a pathogen, they expose C3 binding site and the complement begins its cascade of protein binding