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87 Cards in this Set

  • Front
  • Back
Which antibody is optimal for an agglutination reaction?
Which test uses particulate antigens to detect Salmonella?
Widal Test
Ag's - H(flagella) and O (snowflake,granular)
Which test uses particulate antigens to detect Rickettsial disease?
Weil Felix Test
What term refers to excess antibody inhibiting lattice formation?
What term refers to excess antigen inhibiting lattice formation?
Which agglutination test is used for the detection of primary atypical pneumoniae?
Cold agglutination Test
Antigen + latex particle
Passive Agglutination
What disease is characterized by inflammation-> joint cartilage -> Ab to synovial cavity -> enzymes damage Fc of IgG -> new Ag created -> Ab formed.
Rheumatoid Arthritis; This detects antibody.
The Ab formed against Rheumatoid Arthritis:
Rheumatoid Factor
This passive agglutination technique is used for the antigen detection in various organisms. The test is as follows: unknown culture + dead staph cells = protein A coated with specific enzymes.
What is the name for the passive Hemagglutination technique in which an RBC absorbs a polysaccharide Antigen. The RBC is treated with chemicals to reveal new protein receptors.
Tannic Acid AKA Boyden AKA "Tanned cell" Technique
(if Ag attached passive if Ab attached reverse passive)
An agglutination inhibition test for human chorionic gonadotropic is essentially a test for what?
Pregnancy. No agglutination= postive test.
Which test is characterized by serum + RBC = Hemagglutination
Paul Bunnell
What is the procedure for agglutination by viruses?
Virus + RBC = HA. AB forms complex with virus preventing lattice formation.
In a precipitation the ___ is the precipitin and the ____ is the precipitinogen.
Antibody, antigen
What does a precipitation reaction consist of?
Soluble Ag + Ab
Which test is used to demonstrate toxin production by cornybacterium diptheria?
Elck Test
Explain Immunoelectrophoresis:
Graber and Williams; electrophoresis + precipitin in agar= electrophoretic disperal of Ag and then immunodiffusion reaction.
Which electrophoresis technique is used to reveal Ags in a particular specimen?
Explain counterelectrophoresis:
Nakamura; Ab have little electric charge and migrated toward cathode; Ag have greater mobility and migrate toward anode.
What are some of the advantages of using counterelectrophoresis?
It's fast, sensitive, and you can use large # of speciments.
Explain Rocket Electrophoresis:
This is a combination of immunot electrophoresis and counter electrophoresis. Ag migrates to electrical field applied to gel that contains Ab. Ag combine w/ Ab during electrophoresis-> ppt resembles rocket -> quantitative technique.
Explain Fluorescent Ab Technique:
Ab + fluorescent = fluorescence
Most fluorescents label what?
What are some advantages of using immunofluorescence?
Detection of Ag or Ab is rapid, procedures are shortened, pure cultures are not required, sensitive, low cost.
Explain Flourescytometry:
suspension labeled w/ flourescent monoclonal Ab -> passes across laser beam -> population counted.
Explain Radioimmunoassay:
Very sensitive assay used to measure minute amounts of Ag or Ab.
What are some advantages and disadvantages of radioimmunoassay?
Advantages: sensitive, detection of Ag and Ab
Disadvantages: Expensive equip, safety
Explain Ezyme Linked Immunoabsorbent Assay:
Ab labelled with enzyme + Ag + substrate for enzyme = color change.
What are some ezymes used for elisa?
horseradish, peroxidase, beta galactosidase, phosphatase.
What are some advantages of Elisa?
Safe, stable reagents, reproducibility, inexpensive, many sera @ 1 time.
Explain indirect elisa, double Ab sandwich, and competetive elisa:
indirect: detect of Ab. Ag + Ab (unknown) + (Ab + enzyme) + substrate = color change. Double Ab sandwich: Ab + Ag (unknown)+ unlabelled specific Ab and Ab-enzyme or anti-species + substrate = color change. Competetive: Ab incubated w/ sampe containing Ag -> Ab-Ag mixture added to Ag coated microtiter wells -> the more Ag is sample the less free Ab will be available to bind Ag-coated well.
In general, oraganisms that infect blood are likely to evoke ____ response. Organismas that infect tissues are likely to evoke ___cellular response.
Humoral; cellular
What is the path of bacterial infection?
infection - attachment to cell- proliferation - invasion of tissues - toxin damage to cells.
What is specific immunity for bacterial infections?
phagocytosis= organisms stimulates Ab prod-AgAb complex= increase phagocytosis. Toxin neutralization= Ab+toxin blocks rxn- forms complex with Ab- susc to phago.
What is a toxoid
A detoxified toxin
What is cell mediated response for bacterial infection?
mac engulf and process Ag= sens T cells; some org destroyed by mac others are not. Result = granulomas, cytolytic activity with activated Tc cells.
Explain Ab dependent toxicity:
Ab marks cell and NK cells detect change in cell. This is a type of specific viral immunity
What is neutralization?
Ig binds to virus and blocks the spread of virus to other cells.
What is opsonization?
Viral aggregates + complement; this is easier to phagocytize.
Explain cell mediated viral immunity:
cytolysis by Tc cells.
Explain Immunoparisitology:
Organisms produce chronic disease state; spread by invertebrate vectors.
Explain cell mediated Parasitic Immunity:
protozoans (plasmodium,toxoplasma) = surface Ag = Th and Tdth
Define Affinity:
Strength of a single Ag=Ab bond
Define Avidity:
Strenth at which a multivalent Ab binds to a multivalent Ag.
What are some examples of Bacterial Vaccines?
DPT, TAB, Meningococcal, Hemophilus, pneumococcal, choler, plague, anthrax.
What are some examples of viral vaccines?
HB, Polio, Rabies
Which vaccines are generally killed?
Bacterial vaccines
What are disadvantages of viral vaccines?
infectious virus present, spread of vaccinated person to susceptible person, contaminationg viruses present,genetic change could take place, vaccine susceptible to heat.
Which vaccines are generally attenuated?
Viral vaccines
What are the two stages of graft rejection?
Sensitized (leukocytes from donor move to lymphnodes and stimulate Th cell proliferation)/ effector (Populatation of effector cells migrate to graft to mediate rejection)
Explain Hyperacute graft rejection:
Never accepted by new host.
Explain acute rejection:
first set: appears tissue will take - fever,trans fails- T cells produce lymphokines - blood supply cut- cells die.
2nd set: Retransplant- Ab+NK+T cells - destroy graft blood supply.
Explain Chronic rejection:
Months to years- Walls of blood vessels become blocked by proliferation of smooth muscle cells. Neutrophils then mononuclear cells-capillary endothelium destroyed-blood clots-tissue death.
Explain lymphoagglutination:
Lymphs from donor and recipient tested w/ monoclonal Abs directed against class I Ag.
Explain lymphocytotoxicity teset:
lymphs from donor and recipient tested w/ monoclona Abs directed against class Ig- complement added= lysis
Explain Mixed lymphocyte culture:
In vitro culture of leukocytes from donor or recipient.
Explain two way mixed lymphocyte culture:
Lymphocytes placed in culture - lymphs increase in sized w/in 5 day incubation - this determines if recipient is acting against donor.
Explain one way mixed lymphocyte culture:
Donor lymphocytes are poisoned with mitomycin C- mix with recipient cells-transformed cells become index of recipient response.
What can be used to prevent rejection non specifically?
Corticosteroids (inhibit B and T cells non selectively; Cytotoxic drugs (Act on nucleic acid synthesis/activity); Azathioprine (incorporated into DNA dividing cells-prevent further proliferation).
What is the immune response to tumors?
Nk and cytotoxic T cells
What are some RNA oncogenic viruses?
leukemia, sarcoma, mammary tumor
What are some DNA oncogenic viruses:
Herpes (frog and monkey), Burkitts lymphoma (malig of jaw and face), Hodkins (lymph nodes and spleen), lymphoma
Define neo antigens:
Altered form of previously existing Ag
Explain Grave's disease:
Ab to thyroid stimulating hormone. Can bind to TSH receptor to stimulate secretion of hormone.
Explain Hashimoto's thyroiditis:
Ag= thyroid gland-lymphs and macs= inflammation-goiter-complement mediated lysis- destruction of thyroid cells-hypoactive thyroid.
Explain myexedema:
Ab+cellular rxn-cytotoxic responses-destruction of glandular tissue- thyroid shrinks.
Explain Myesthenia gravis:
Muscle weakness-skel muscles fatigue- auto ab to acetylcholine receptors protein- reduction in # of receptors.
Explain autoimmune anemias
Pernicious (intestinal protein), hemolytic anemia (ab to RBC Ags binds to RBC)
Good Pasture's Syndrome
Kidney disease. Ab against glomerular basement.
Explain Insulin Dependent Diabetes:
Autoimmune rxn to insulin producing cells; destroys b cells; decrease in insulin production; increase in blood glucose.
Post-strep diseases:
Kidney and heart; cross reactive type of Ab. Group A strep contain Ag that are cross reactive w/ kidney and heart.
Explain Systemic lupus erythematous:
Development of autoAbs against nucleic acids; Auto Abs form immune complexes that deposit in organs-inflamm rxns-destruc of cells in organs=damage to glomerular nephron-threatening kidney failure
Explain multiple sclerosis
Myelin sheaths destroyed-slower nerve impulses- Ab + complement=destruction of myelin sheath. Dia: increased IgG in myelin sheath.
Explain Rheumatoid Arthritis:
Inflammation of connective tissue-joints=may lead to death.
Explain Scleroderma:
Tightening of skin= over production of collagen in connective tissue.
Explain Bruton type hypogammaglobulinemia:
Sex linked disease; male infants suffer from chronic bact infection; B cells fail to develop.
Explain DiGeorge's syndrome:
Person born with little or no thymus gland. T cells markedly reduced. B cells are present, but Ab levels are very low. Not inherited like Nezelof's.
Explain Nezelof's syndrome:
Inherited thymic disorder; T cell def disorder that results in abnormal Ig sythesis. Decrease in T cells but not be cells.
Explain Wiskiott-Aldrich syndrome:
bleeding-reduced platelets-recurring inf-eczema-fatal injection of lymphoid malignancy.
Explain leprosy:
T cells depressed- lymphocytes not responsive to mitogens.
Explain Bare lymphocyte syndrome:
No class II MHC molecules
Explain Chronic granulomatous disease:
Phagocytic disfunction of certain enzymes. cells fail to generate toxic species.
Explain Chediak-Higashi syndrome:
Fragile lysosomal membranes which do not degranulate properly.
Describe the 3 types of anaphylaxis:
local (allergies;mild; sneezing,itching,food); systemic (severe; life threatening, shock), Cutaneous (skin rxn-rapid-few minutes)
What are some mediators involved in Type I hypersens?
Histamine-released by cell degranulation-vasodilation, musc contraction. Serotonin-same as histamine but seen in rats. SRS-A, ECF-A (in nasal secretions), Prostaglandins, Cytokines (released by mast cells and eosinophils.
Describe Type II hypersensitivity:
Rxns against blood cells. Rxns against tissue Ags. Transfusion Rxn-incompatible blood.