Microbiology Exam 3

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AVAILABLE iron, if blood cells lyse, there will be more available iron
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blood is normally sterile but can handle moderate number of microorganisms. blood is low in ( ), which is needed for bacteria to thrive.
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blood poisoning, or sepsis
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if defenses fail (phagocytic cells in blood and lymph) uncontrolled proliferation of bacteria in the blood is called ( )
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lymphangitis
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sepsis is often accompanied by ( ), inflamed lymphatic vessels visible as red streaks along appendages from the infection site to a lymph node
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release of cytokines (inflammatory mediators, promote faster immune response)
fever
chills
rapid breathing
rapid heart rate
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what are signs/symptoms of sepsis?
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severe sepsis
septic shock
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if sepsis proceeds to a drop in blood pressure and dysfunction of organ/s ( ) occurs
if the low blood pressure cannot be controlled, ( ) occurs
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Pseudomonas aeruginosa: Gram – bacterium
Streptococcus pneumoniae: Gram + bacterium
Aspergillus fumigatus: fungus
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three sepsis pathogens
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gram negative
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is septic shock most often caused by gram negative or gram positive bacteria?
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Escherichia coli
Pseudomonas aeruginosa
cell walls of these bacteria release endotoxins upon release
less than one-millionth of a milligram of endotoxin is enough to cause septic shock
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gram negative sepsis is most often caused by what?
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nosocomial infection
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infections that result from treatment in a hospital
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Streptococcal and staphylococcal infections
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causes of toxic shock syndrome
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Enterococci – inhabitants of the skin and human colon
Enterococcus faecium
Enterococcus faecalis
Streptococcus pneumoniae
all are Gram + cocci, facultative anaerobes
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leading cause of nosocomial infections (infections resulting from treatment in a hospital)
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Streptococcus pyogenes
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puerperal fever is usually due to ( )
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puerperal sepsis
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also known as childbirth fever – a nosocomial infection
infection of the uterus after childbirth or an abortion -> progresses to an infection of the abdominal cavity (peritonitis) then to sepsis
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rheumatic fever
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early in the 20th century, this killed more school-aged children in the US than all other diseases combined
leading cause of heart disease in the world in people younger than 50
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rheumatic fever
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streptococcal infections (usually Streptococcus pyogenes)
usually children (4 to early teens), often following strep throat
an autoimmune disorder
arthritis, fever, joint nodules, valve damage
may lead to heart or kidney disease – or death
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vegetation
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clot on a heart valve
bacteria (or their toxins) damage the collagen of the valves
causes fibrin to be released
the bacteria can attach to damaged valves (fibrin)
immune cells contribute and make them larger
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endocarditis
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inflammation of the endocardium
it usually effects the valves (vegetations)
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may be the result of rheumatic fever or a genetic problem
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subacute bacterial endocarditis
acute bacterial endocarditis
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2 main types of endocarditis
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subacute bacterial endocarditis
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fever, malaise, heart murmur, hematuria
slow developing
causes: streptococci (those common in oral cavity), staphylococci, enterococci
often arise from teeth or tonsil infections that become systemic
more common and less debilitating than ABE
can strike anyone
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acute bacterial endocarditis
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usually Staphylococcus aureus in origin
strikes rapidly
can infect/destroy normal or abnormal heart valves quickly
death in a few days or weeks if untreated
more common among elderly, IV drug users
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Bartonella henselae
Gram – bacillus
anaerobe
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causes cat scratch disease
inhabits the interior of some feline RBCs
lymph node swelling, fever, papule at infection site, malaise
69% of dog bites become infected if not cleansed well
various genera, such as Pasteurella, Clostridium, etc
local swelling, severe pain, possibly sepsis
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anatomic and physiologic barriers
inflammation
phagocytosis
complement system (alternate pathway)
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components of the nonspecific (innate) immunity
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barriers that limit invasion, spread, and replication
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anatomic and physiologic barriers
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after tissue damage, blood vessels increase in diameter (vasodilation) and increase in permeability
increased permeability allows substances normally in the blood to pass out of the blood more freely
1) erythema (due to increase in blood flow)
2) heat (due to increase in blood and more rapid metabolic reactions)
3) edema (increased permeability, fluid moves from blood to tissue space)
4) pain (injury to nerve fibers or increase in pressure from increased edema, increased cytokines, toxin from bacteria cause pain)
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4 characteristic signs of inflammation
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histamine
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increased vasodilation, increased permeability
released by mast cells in connective tissue
released by basophils in the blood
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prostaglandins
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intensify the effects of histamine
released by local tissues
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leukotrienes
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increase permeability
released by mast cells and basophils
also function in adherence of phagocytes to pathogens
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cytokines
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released by monocytes, macrophages, lymphocytes, etc
regulators of inflammatory response
attract leukocytes, initiate fever, etc
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complement (can be specific and non specific)
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increase vasodilation, increase permeability
stimulates histamine release, attracts neutrophils, promotes phagocytosis
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1) bacteria and other pathogens enter wound
2) platelets from blood release blood clotting proteins at wound site
3) mast cells release factors that mediate vasodilation and vascular constriction. delivery of blood, plasma, and cells to injured area increases
4) neutrophils secrete factors that kill and degrade pathogens
5) neutrophils and macrophages remove pathogens by phagocytosis
6) macrophages secrete hormones called cytokines that attract immune system cells to the site and activate cells involved in tissue repair
7) inflammatory response continues until the foreign material is eliminated and the wound is repaired
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the inflammatory response
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neutrophils
macrophages
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phagocytosis is initially done by ( ) and eventually by ( )
destroys the whole organism, mainly bacteria
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the complement system consists of over 20 different plasma proteins
2 pathways are activated: nonspecific and specific immunity
nonspecific (alternate pathway) is usually activated by microbial surfaces and cell surface components (lipopolysaccharides)
doesn’t involve antibodies
stimulates histamine release from basophils, platelets, mast cells
causes cytolysis
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actions of the alternate pathway (nonspecific immunity complement system)
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BEN: basophils, eosinophils, neutrophils…mast cells
granulated
fragments that hold the nucleus together (don’t have many nuclei, just one that is connected)
function: fight off infection by phagocytosis or by destruction of the antigen, may secrete something to destroy the antigen
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examples of polymorphonuclear cells and their function
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monocytes, macrophages, dendridic cells
function: present antigens, without these cells antigen wouldn’t be presented for the appropriate cells to respond (lymphocytes respond to the antigens)
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examples of antigen presenting cells and their function
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innate: rapid, nonspecific, polymorphonuclear cells and antigen presenting cells, preformed effectors with limited variability, no memory or increase in response upon secondary exposure
adaptive: slow, specific, lymphocytes, there are an array of cells with specific receptors that are highly selective, memory and maturation of secondary response
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compare and contrast the innate and adaptive immune response
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they are derived from hematopoietic stem cells in the bone marrow
they differentiate into myeloid cells (first line of defense) or lymphoid cells (second line of defense)
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monocytes give rise to macrophages (in the tissue) and dendritic cells. monocytes, macrophages, and dendritic cells are antigen presenting cells
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in the blood stream they are a basophil, in the tissue they are mast cells
monocyte in the blood stream, macrophage in the tissue
B cells differentiate into plasma cells in the tissue
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where are immune system cells derived?
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neutrophils
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short lived myeloid cells
ingest, kill, and digest microbial pathogens
first to inflammatory sites
granules contain antimicrobial agents such as hydrogen peroxide, lysozymes, and lactoferrin (iron chelator) to break down bacterial cells walls
these cell’s death contribute to the formation of pus
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eosinophils
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myeloid cell
mediate allergic reactions and defense against helminths
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basophils
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myeloid cell
mast cells are tissue counterpart
produce cytokines in defense against parasites and are responsible for allergic reaction
secrete primary mediators – histamine
and secondary mediators – leukotrienes, prostaglandins
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liver, brain, skin, bone, lungs
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what organ systems have fixed macrophages?
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monocyte
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myeloid cell
macrophages are tissue counterpart
phagocytosis and intracellular killing
antigen presentation to T cells
recruit other immune cells through cytokine production
specialized macrophages found in the liver, brain, bone, skin, and lungs
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dendritic cells
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differentiated macrophages
act as antigen presenting cells to activate helper T cells, B cells, cytotoxic T cells
in most organs
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B lymphocytes
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lymphoid cells
differentiate into plasma cells to secrete immunoglobulin glycoproteins that bind antigens with a high degree of specificity
provide humoral immunity
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T lymphocytes
without helper T cells, nothing would happen b/c T cells stimulate B cells to differentiate into plasma cells and make antibodies
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lymphoid cells
immature thymocytes differentiate in the thymus
cell mediated immunity
help B cells produce immunoglobulins
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Helper T cells
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lymphoid cells
express CD4
regulators of delayed-type hypersensitivity reponses
ASSIST IN THE STIMULATION OF B CELLS
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Cytotoxic T cells
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lymphoid cells
express CD8
cytotoxic against tumor cells and host cells with intracellular pathogens
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natural killer cells
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lymphoid cell
large granular lymphocytes that kill tumor cells and pathogen infected cells
enhanced by interferon and interleukin
lack the major B and T cell markers
kill by direct and antibody dependent cytotoxicity
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microvilli
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( ) allow T cells to stick to endothelial cells. migrating cells then emigrate between cells
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lymphoid organs
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tissues where leukocytes mature, differentiate, and proliferate
made of epithelial and stromal cells arranged in capsulated organs or accumulations of diffuse lymphoid tissue
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primary lymphoid organs
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sites of lymphopoiesis
where B and T cells differentiate from stem cells into antigen recognizing cells
fetal liver and adult bone marrow and thymus
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secondary lymphoid organs
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where antigen driven proliferation and differentiation of B and T cells occur
spleen, lymph nodes, MALT, tonsils, Peyer’s patches, appendix
ARE NOT encapsulated
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thymus gland
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primary lymphoid organ
gland where T lymphocytes distinguish between self and non-self antigens: immuno-incompetent cells differentiate into immuno-competent cells
they will acquire specific receptors that allow them to break down pathogens or stimulate B cells
cells are maturing, but will not be fully mature until they reach a secondary lymphatic organ
the outer cortex contain thymocytes (immature cells that will mature to lymphocytes). About 98% of the thymocytes that are produced will be phagocytized (macrophages destroy the ones that aren’t capable of distinguishing self from non-self)
in the medulla are mature lymphocytes that will be distributed to other parts of the body
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spleen
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secondary lymphoid organ
filter for blood
red pulp: vascular sinuses with macrophages
white pulp: T and B cell area, germinal centers with macrophages and dendritic cells that present antigen to lymphocytes, B cells become plasma cells
responds to blood borne pathogens, whereas lymph nodes response to lymph-borne pathogens
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destruction by macrophages of what is in the blood as it passes through the spleen
BIGGER ROLE OF MACROPHAGES IS BREAKING DOWN OLD ERYTHROCYTES
helps to recycle hemoglobin
STORES erythrocytes and platelets
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red pulp functions
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helps in the initiation of the immune response by presenting antigens to the lymphocytes
activation of the immune response
antigen/antibody complexes will stimulate T cells to stimulate B cells to mature into plasma cells so antibody secretion is possible
destruction of the antigen
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white pulp functions
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spleen is the largest secondary lymphatic organ
lack of a spleen will affect antibody production. by minimizing the number of potential T and B cells, there will be less antibody production
body will have to rely more on other secondary lymphatic organs like the tonsils
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how does the lack of a spleen affect immune cell function, and what implications does this have for immune responses to infective agents?
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children do not have a well developed immune system
there will be a lack of antibody production and lack of immunological memory
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why does loss of a spleen represent more of a clinical problem in children than in adults?
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lymph nodes
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secondary lymphatic organs
filters antigen and debris from lymph
macrophages and dendritic cells cleanse lymph through phagocytosis
T cell and B cell maturation occurs
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mucosa associated lymphoid tissue
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what does MALT stand for?
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mucosa associated lymphoid tissue (MALT)
tonsils
Peyer’s patches
appendix
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secondary lymphatic organs
cellular aggregates in the lining of the respiratory and digestive tracts
resident intraepithelial lymphocytes
strategically located to initiate an immune response
break down pathogens or deliver pathogens to the lymph nodes if the infection rate is high
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cell-mediated immunity (T cells) and humoral immunity (B cells)
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adaptive (acquired) immune response involves what 2 kinds of immunity?
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T lymphocytes (T cells) can lyse infected target cells or secrete immunoregulatory factors following interaction with antigen presenting cells to combat intracellular viruses and organisms
mature T cells express T cell receptors specific for an antigen
All T cell receptors expressed by a single T cell are specific for the same antigen
The T cell receptor is in association with coreceptors (CD4/CD8) that allow it to recognize antigens with major histocompatibility complex Class I or II on target cells
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mechanism of cell-mediated immunity
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Omenn’s syndrome
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this is a form of severe combined immunodeficiency
absence of germinal centers in lymph nodes and replacement with a diffuse infiltrate of large cells with abundant cytoplasm
abnormal intra-thymic T cell development plus inefficient and/or abnormal generation of T cell receptors
deficiency of B-cells and receptors (antibodies)
autosomal recessive gene
treatment is bone marrow transplant, immunosuppresant drugs, antibiotics
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T cells continue to differentiate after leaving the thymus, after encounter with a specific antigen in the lymph nodes/spleen/MALT
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maturation of T cells
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T helper cells
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express the CD4 co-receptor
recognize antigen complexed with MHC II on B cells, macrophages, or other APCs
activate memory T helper cells and cytokine secreting cells; stimulate B cells
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cytotoxic T cells
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express the CD8 co-receptor
dependent upon MHC I on APCs
are cytotoxic against tumor cells and host cells with intracellular pathogens by apoptosis
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B cell receptors
T cell receptors
major histocompatibility complex
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three groups of molecules that specifically recognize foreign antigen for the adaptive immune system
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major histocompatibility complex
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a gene locus that codes for histocompatibility antigens
these antigens are cell surface glycoproteins that are critical to immune cells
antigen is recognized by T cells when it is presented in complex with proteins of this.
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endogenous (cytoplasmic) antigen processing
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Class I MHC molecules are found in ALL nucleated cells
participate in antigen presentation to CD8 cytotoxic T cells
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virus enters cell
virus is broken down into peptides so that portions of the virus can be presented on the surface of the cell
rough endoplasmic reticulum will make MHC I
complex formed with MHC I and the parts of the virus
virus will be recognized by cytotoxic T cells
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exogenous (endosomal) antigen processing
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MHC II molecules are found on antigen presenting cells (macrophages, dendritic cells, B cells)
antigen presentation to CD4 helper T cells
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portion of cell wall/toxin goes into the cell
rough endoplasmic reticulum produces MHC II
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DiGeorge syndrome
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a chromosomal abnormality that causes a lack of thymic tissue
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cytokines
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proteins that induce characteristic cellular responses when they bind to specific receptors on their target cells
play a role in the innate, cell-mediated, and humoral immune response
ex) interleukin, tumor necrosis factor
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innate immune response: cytokine = IL-1, source = macrophage, actions = fever
humoral immune response: cytokine = IL-5, source = T helper cell, actions = IgA synthesis
cell-mediated immune response: cytokine = IL-12, source = macrophage, actions = stimulates formation of helper T cells
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give an example of a cytokine that plays a role in the innate, humoral, and cell-mediated immune response, its major source, and its actions
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drop in blood pressure, shock, fever, blood clotting
endotoxin stimulation of macrophages after gram negative bacterial infection -> septic shock
a massive release of cytokines can be due to superantigen stimulation of T cells by bacterial toxins -> toxic shock
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what can an overexpression of cytokines lead to?
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Trypanosoma cruzi
chagas disease
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what bacteria can cause a decrease in cytokine release leading to immune suppression?
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to bind antigen and inactivate it
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what is the main function of immunoglobulins (antibodies)?
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expressed on the surface of B-cells
expressed on the surface of terminally differentiated B-cells called plasma cells
as soluble proteins in the blood
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where are immunoglobulins (antibodies) found in the body?
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IgD
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Less than 1% in serum
with IgM, major immunoglobulin expressed by mature B-cells
functions in activation of B-cells by antigens
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IgG
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about 80% in the serum
protects fetus
neutralizes bacterial toxins and viruses
complement activator
4 subclasses
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IgE
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less than 1% in serum
binds to allergens
mediates hypersensitivity reactions such as asthma, hives, hay fever by inducing degranulation of basophils, mast cells
protects against parasitic infections
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IgA
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about 10-15% in serum
main immunoglobulin in external secretions (tears, saliva, breast milk, mucus)
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IgM
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about 5-10% in serum
first immunoglobulin produced in a primary response to an antigen
has 10 antigen binding sites
activates complement pathway
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secretion of immunoglobulins occurs only after antigenic stimulation of membrane-anchored immunoglobulins on the surface of the B-cell
differentiation occurs in the germinal centers of lymph nodes, spleen, or MALT (tonsils, Peyer’s patches)
this requires antigenic recognition and T-cell cytokines
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mechanism of humoral immunity
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epitope
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the molecular region on an antigen recognized by an antibody is called an antigenic determinant, or ( )
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antigen
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any substance recognized by the immune system
classes are lipids, proteins, carbohydrates, and nucleic acids
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immunogen
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any substance that can evoke an immune response
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true
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true or false
all immunogens are antigens, but not all antigens are immunogens
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[image]
the antibody response on the second contact with the antigen is more rapid and more intense
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what is the difference between primary and secondary responses to a pathogen based on immunological memory?
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multiple myeloma is also called plasma cell myeloma
plasma cells grow out of control and form tumors in the bone marrow
the excess growth of plasma cells interferes with the body’s ability to make RBCs, WBCs, and platelets which causes anemia
these patients are more susceptible to infection b/c there is too much of one type of plasma cell.
will be protected by the antibody that is secreted by the plasma cells (ex. IgG), but will not have protection against anything else
won’t be able to differentiate any new B cells b/c plasma cells have replaced normal bone marrow
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what is the immunologic basis for multiple myelomathese patients have high antibody levels, but why are they considered more susceptible to bacterial infections?
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complement system
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system of over 30 serum and cell surface proteins that form an enzymatic cascade and are involved in immunity and inflammation
alternate and classical pathways
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alternate pathway
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part of the complement system
most commonly activated by microbial surfaces or cell components (ex. lipopolysaccharides)
generates early innate response
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classical pathway
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part of the complement system
activated by ag/ab complexes containing IgM or IgG
major effector of humoral immunity
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IgG and IgM
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2 antibodies involved in the complement classical pathway
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Membrane Attack Complex (MAC) acts as a molecular drill to puncture cell membranes
complement cleavage products promote opsonization (enhancement of phagocytosis), inflammatory responses, degranulation, etc
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biological activities of complement products
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liver
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most complement proteins are produced by the…
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complement interacts with IgM and IgG, binding to pathogen surface
MAC (membrane attack complex) makes pore channels -> lysis of target cells
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[image]
explanation of #1
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complement binds to pathogen, interacts with receptor on phagocytes, enhancing phagocytosis
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[image]
explanation of #2
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specific complement on the surface of the antigen
stimulates degranulation
destroys the antigen
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[image]
explanation of #3
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specific complements help solubilize and clear immune complexes and will enhance transport to the liver and spleen for further destruction
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[image]
explanation of #4
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coating of antigen with complement facilitates their delivery to germinal centers rich in B cells
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[image]
explanation of #5
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genetic factors
cross reactivity of antimicrobial antibodies with host tissues
polyclonal activation induced by tumors or infection (multiple myeloma)
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causes of autoimmune diseases
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multiple sclerosis
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autoimmune disease where T cells recognize part of the mylin sheath as foreign
autoreactive T cells that recognize targeted self antigens leading to direct damage
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active
naturally acquired active immunity -> antigens enter the body naturally, body produces specific lymphocytes and antibodies
artificially acquired active immunity -> antigens are introduced in vaccines, body produces antibodies and specialized lymphocytes
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what type of acquired immunity occurs when a person is exposed to antigens and the immune system responds?
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passive
naturally acquired passive immunity -> antibodies pass from mother to fetus via placenta or to infant via breast milk
artificially acquired passive immunity -> preformed antibodies in immune serum introduced by injection
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what type of acquired immunity is acquired when antibodies are transferred from one person to another?
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inactivated bacterial toxin (toxoid)
killed microbes
living but attenuated (weakened)
parts such as capsules
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in what 4 ways can a vaccine be produced?
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hypersensitivity
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antigenic response beyond the “norm”
allergies
individuals who have been sensitized by previous exposure to an allergen; upon reexposure immune system reacts in a damaging way
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anaphylaxic reactions
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Type 1 hypersensitivity
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cytotoxic reactions
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type II hypersensitivity
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immune complex reactions
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Type III hypersensitivity
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cell mediated reactions
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type IV hypersensitivity
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type I anaphylaxic reaction
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involves an humoral immune response
refers to the reaction when certain allergens combine with IgE antibodies
can be a systemic reaction (shock, difficulty breathing, potentially fatal) or localized reaction (hives, hay fever)
IgE’s bind to mast cells, basophils causing degranulation
mediators: histamine, leukotrienes, prostaglandins
mediators attract neutrophils, eosinophils
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systemic anaphylaxis
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anaphylaxis that occurs due to the release of mediators that cause blood vessels to enlarge, drop in BP (shock)
usually in response to injected antigens
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localized anaphylaxis
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anaphylaxis usually caused in response to ingested or inhaled allergens
itchy eyes, sneezing

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