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organisms in/on your body |
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there a cost to you and a benefit to the parasite |
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Koch's Postulates (experiment) |
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i. Experiment: isolate colony, identify org, inject the org into a live animal, disease is reproduced in the new animal, isolate the pathogen from the animal, identify the microbes |
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Exceptions to Koch's Postulates |
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ii. Exceptions: 1.reinfection may not work 2. Different response in diff animals 3. Virus, cell line 4. Obligate intracellular pathogens are difficult to isolate |
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1950 mapped the spread of Cholera in London -> infectious agents can travel in H20, fecal/oral Used stats, personal accounts, history Epidemiology public health |
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Signs, symptoms, syndromes |
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How a disease acts in a host/pop |
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Communicable Contagious Noncommunicable |
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a fraction of a population that contracts it during a period of time |
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the fraction of the population having the disease at a specific time |
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Only occasionally (typhoid in US) |
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Constantly present (common cold) |
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many people acquire in a short time |
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develops rapidly, lasts short time (influenza) |
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develops slowly, less severe, likely to recure long periods (mono |
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in between acute and chronic |
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causative agent remains inactive for a long period of time (shingles) |
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pathogen limited to small area of the body (boil) |
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spread throughout the body in blood or lymph (measles) |
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agents of a local infection spread to specific parts of the body (teeth to gums, tonsils) |
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bacteria replicating in the blood |
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presence of toxins in the blood |
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presence of viruses in the blood |
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acute infection that causes the initial illness |
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opportunistic pathogen after the primary infection has weakened the host |
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no noticeable illness (carrier) |
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place where pathogens live humans animals soil water |
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contact: direct, indirect, droplets vectors: mechanical and biological vehicle: water air |
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most acute signs/symptoms |
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peak point; death if immune responses/meds don't work |
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capabilities of pathogens |
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i. Maintain a reservoir ii. Leave a reservoir (transmission route) iii. Adhere to a host iv. Invade a host v. Evade host defenses vi. Colonize and multiply in the host vii. Exit the host and return to the reservoir (or infect a new host) |
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Glycocalyx (capsule)- very sticky Pili, fimbriae (attach via receptor) Protein M (streptococcus): sticky component |
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the infectious dose required to infect 50% of the hosts in the study |
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the lethal dose required to kill 50% of the host in the study |
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chemicals or structures produced by the pathogen that cause direct damage to the host |
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Types of virulence factors |
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Definition
Hyaluronidase: enzyme breaks down hyaluronic acid (tissue cement)(Staphylococcus) Leukocidins: destroy WBCs (Stapylococcus) Hemolysins: lyse RBCs (B streptococci) Coagulases: produce clots to block antibodies (S. aureus) Streptokinases and kinases: break down fibrin in clots- allow it to invade more tissue Collagenase: breaks down connective tissue (Clostridium) IGA proteases: destroy antibodies and evade (Neisseria) Invasins: use cytoskeleton filaments to make a cage for protection (E.coli, Salmonella) Toxins: more indirect damage |
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i. Exotoxins: produced inside the cell and are secreted outside 1.AB toxins: very specific damage a.Cytolytic: cells lysis and cell death (diphtheria toxin b.Neurotoxic (botulinum toxins) c.Enterotoxic: cause gastroenteritis 2.Membrane disrupting 3.Superantigen: stimulate a large number of immune response reactions, produced by Streptococci & Staphylococci |
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1. Gram negative bacteria produce lipopolysaccharides as part of the out layer of the cell walls. The Lipid A components are called endotoxins. They are cell-bound and released in large numbers only when the cells lyse |
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Etiological agent: Stapylococcus aureus Mode of transmission: direct contact Treatment: IV antibiotics |
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i. Etiological agent: Mycobacterium ulceras Reservoir: water Mode of transmission: unknown Treatments: antibiotics |
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Etiological agent: Chlamydia trachomatis Mode of transmission: direct contact, fomites (towels), vector (flies) Treatments: antibiotics, eyelid surgery Epidemic: 50 countries in Africa, Asia, Middle East |
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Etiological agent: Staphylococcus aureus and Streptococcus pyogenes Mode of transmission: direct contact or fomites Treatment: antibiotic cream or pills |
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Necrotizing faciitis (skin) |
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Definition
Etiological agent: exotoxins A and B of Streptococcus pyrogenes Transmission: direct contact Treatment: antibiotics, excision of damaged tissue, hypobaric chamber |
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African Trypanosomiasis (nervous system) |
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Definition
Etiological agent: Trypanosoma brucei gambiense & Trypanosoma brucei rhodesiense Vector: tsetse fly Transmission: bite of the tsetse fly Treatment: chemtheraputic drugs Epidemic: Africa |
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Etiological agent: lyssavirus (RNA) Reservoir: wild animals Transmission: direct contact (wound) Treatment: post-exposure prophylaxis Epidemic: developing countries like Asia and Africa |
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Botulism (nervous system) |
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Definition
Etiological agent: Clostridum botulinum Toxins A, B, E (neurotoxins) Reservoir: soil, animals Transmission: ingestion of contaminated foods or direct contact (wound) Treatment: Botulinus antitoxin |
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Etiological agent: Clostridium tetani (toxins) Reservoir: soil, animal intestinal tracts, and feces Transmission: wound contact, animal bites Treatment: antitoxin, vaccine |
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Etiological agent: Poliovirus Mode of transmission: fecal oral Treatment: no cure, vaccine Epidemic: 1940s and 50s |
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Bacterial endocarditis (cardiovascular) |
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Definition
Etiological agent: anything that causes bacteremia: Streptococcus, Staphylococcus, Enterococci Mode of Transmission: direct contact with wound (brushing teeth) Treatment: antimicrobial therapy or surgery Epidemic: 2009 Nottingham University Hospital heart valve patients |
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Etiological agent: Borrelia burgodorferi Reservoir: animals Mode of transmission: direct or fomites or respiratory droplets Treatment: penicillin and corticosteroid |
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Etiological agent: Clostridium perfringens Reservoir: soil Transmission: open wound Treatment: surgery, sterilization, O2 |
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Etiological agent: Bacillus anthracis (2 exotoxins) Reservoir: soil Transmission: inhalation of spores or direct contact with soil/animals Treatment: antibiotics, vaccine Epidemics: 2001 bioterrorism |
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Cornyebacterium diphtheriae (exotoxin) Reservoir: humans/animals Transmission: respiratory droplets, contaminated drinks Treatment: vaccines, antitoxin, antibiotics |
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Etiological agent: Mycobacterium tuberculosis Reservoir: humans Transmission: respiratory droplets Treatment: antibiotics Epidemic: 2 mill ppl/year |
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Etiological agent: Histoplasma capsulatum Reservoir: fungus that grows in soil Transmission: inhalation of airborne fungal spores Treatment: antifungal meds |
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Whopping cough/ pertussis (resp) |
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Definition
Etiological agent: Bordetella pertussis (cytotoxin) Transmission: respiratory droplets Treatment: antibiotics, vaccine Epidemic: Washington 2012, Cali 2010 |
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Etiological agent: Group A Streptococcus pyogenes (exotoxins A, B, C & M protein) Reservoir: Humans Transmission: respiratory droplets or direct contact Treatment: antibiotics |
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Etiological agent: paramyxovirus of the genus Rubulavirus Reservoir: humans Transmission: respiratory droplets Treatment: vaccine (preventative) Epidemic: 2006 Midwest college students |
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Typhoid fever (digestive) |
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Definition
Etiological agent: Salmonella typhi Reservoir: water Host: humans Transmission: fecal oral Treatment: vaccine (preventative) Epidemics: 17 mill ppl infected each year |
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Etiological agent: Hepatitis C virus Reservoir: humans Transmission: blood to blood Treatment: antivirals Epidemic: 3.2 million ppl in the US |
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Gastric ulcers (digestive) |
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Definition
Etiological agent: Helicobacter pylori Mode of transmission: fecal oral Epidemic: 90% of population in Brazil |
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Etiological agent: Vibrio cholerae (exotoxin A, B) Mode of transmission: fecal oral Treatment: rehydration and salt; antibiotics Outbreaks: Feb 2012 Sierra Leone 18500 cases |
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Etiological agent: Treponema pallidum Mode of transmission: sexual contact Treatment: penicillin Epidemic: 10-12 million ww. |
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Leptospirosis (urogenital) |
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Definition
Etiological agent: Leptospira interrogans Reservoir: rodents/animals Mode of transmission: direct contact with soil, water or plants contaminated with urine Treatment: antibiotics Epidemics: Caribbean, latin America |
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Pyelonephritis (urogenital) |
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Definition
Etiological agent: E. coli, Streptococcus faecalis and Staphylococcus aureus Reservoir: Humans/animals Portal of entry: Urethral opening Treatment: antibiotics Epidemic: neonatal ward in Sweden |
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Definition
Etiological agent: Candid albicans (toxins) Transmission: direct contact Treatment: topical drugs/antifungals/oral meds |
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Genital herpes (urogenital) |
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Definition
Etiological agent: Herpes simplex virus 1 & 2 Mode of transmission: sexual contact Reservoir: humans Treatment: incurable; antivirals Epidemic: 16.2% adults in US; 65-90% world wide |
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Definition
born with; non-specific (ex: skin, barriers); target all non self |
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Innate immunity: 1st line of defense: physical and chemical |
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Definition
Physical: skin; mucous linings; flushings, cilia; flow of urine; movement of food Chemical: saliva (lysozyme), skin secretions |
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Innate immunity second line of defense |
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Definition
Blood: formed elements (cells) and soluble proteins Formed elements= platelets (clotting; macrophage (phagocytosis); dendritic cells (phaocytosis), granulocytes: eosinophils (allergy), neutrophils (phagocyte), basophil (allergies and worms) |
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Definition
differential white blood cell count |
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Soluble proteins (where are they made, what do they do?) |
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Definition
Made in the liver (1) Cytolysis (2) Coating a cell= opsonization (a) Captures bacteria to enhance phagocytosis (3) Cascade effect (several proteins act together) |
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Definition
cell secretions that help communicate with immune cells |
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Toll-like receptors; Pathogen Associated Molecular Patterns (PAMPs) |
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Definition
(1) Your TLR can recognize LPS (pathogen specific substance) and release cytokines which target the liver and activate acute phase proteins (APP) |
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acute phase proteins (APP) |
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Definition
activate phagocytes, migrate MAC, PMNs |
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Definition
Very rapid, nonspecific Signs/symptoms: red, swollen, heat, painful, (loss of function) |
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Definition
APP are triggered and travel to the site; cytokines and chemicals cause: vasodilation, phagocytosis, repair of tissue |
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Complement serum proteins |
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Definition
Opsonization: coating, cytolysis |
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Definition
Cells being attacked by viruses release INFs to help protect neighboring cells against infection |
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Definition
Produced in the liver (1) Can opsonify (2) Circulate in the body |
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Definition
Host has to be exposed to something foreign (be sensitized) before you have a response |
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Definition
WBCs derived from a lymphocytic stem cell line |
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Definition
in-bone marrow: humoral immunity (circulate in the blood) |
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processed in the Thymus: cell-mediated immunity |
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MHCs: Major histocompatability markers (on nucleated cells only) |
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Definition
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active; produce proteins called antibodies |
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Definition
Agglutinate: make a big lattice of bacteria cells and destroy the antigens in the liver Opsonization (coating) Antibodies function as a “tag” to stimulate phagocytosis Phagocytosis Neutralize toxins via complexing it with antibodies Integrate w/ cell-mediated (T-cells) |
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Memory b-cells: Quiescent |
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Definition
Clones that have been “sensitized” by an antigen but are inactive until it comes in contact with the antigen again |
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Cell-mediated immunity: T lymphocytes |
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Definition
Must be presented to the antigen (don’t circulate) by an APC |
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APC: antigen presenting cell |
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Definition
Macrophage, dendritic cell (some are neutrophils and B cells) |
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Definition
Interleukins; Regulators, Produced Th1 and Th2 |
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Definition
Secrete IL-2 in order to stimulate both WBCs and self-proliferation Create active clones and memory clones |
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Definition
Stimulated by an APC and antigen. Clones secrete IL 4, 5 Stimulate B cells which produce antibodies |
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Definition
cytokines, perforins (kill via lysis) Produce Tc cells |
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Definition
Create memory and active clones (secrete the cytotoxins) |
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Definition
An exaggerated immune response May come about via too many antibodies, t-cells or antigens |
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Definition
1913 Nobel Prize in Medicine TB serum, injected into human, caused anaphylactic shock |
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Type 1 Hypersensitivity: Anaphylaxis |
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Definition
B-cells and IgE antibodies Mast cellss (linings/mucous) and basophils (granuols) Antigens (a)Pollen: inhale (upper respiratory): localized (b)Food: eating (systemic) (c)Bites: systemic |
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Type 2: Cytotoxic hypersensitivity: Cell Bound |
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Definition
B cells -> IgG and IgM Involves cell bound antigens ex: those on RBC like RH factors Eg: transfusion mistake or hemolytic disease |
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Definition
mom antigen and baby antigen are different; active=complement proteins (perforins) that kill/lyse developing embryo |
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Type 3: Immune Complex: Not cell bound |
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Definition
Soluble antigens B cells-> Ig G and IgM (forms big complexes) Complement proteins Disease: Glomerulonephritis (kidneys) |
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Glomerulonephritis (kidneys) |
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Definition
Complexes form in the glomerulous : stops filtering and ALERTS an inflammatory response -> release of complement proteins -> WORSE |
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Type 4: Delayed Type ( 2days- weeks) |
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Definition
T cells (Tc) Ex: Latex dermatitis (rash) Poison Oak systemic rash/swelling |
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Autoimmune Responses (Hypersensitivity) |
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Definition
Loss of self recognition Response of AB/T cells against own antigens (MHC) |
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Causes of autoimmune responses |
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Definition
i) Infections: mimicry ii) Antigen: not exposed to the body (ex: inside of eye) iii) Hormonal |
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4 most common Autoimmune Responses |
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Definition
Myasthenia Gravis: IgG blocks nerve synapses causing paralysis (type 2 or 4) Rheumatoid arthritis: 2 mill mainly women;IgM and IgG and complement form complexes @ joints; virus infections may be the cause (type 3) Lupus: 200,000 to 1.5 million AB vs. cell nuclei (type 3) Insulin dependent diabetes: 1.6 million (Type 4) |
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Autoimmune disorders/deficiencies |
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Definition
innate-born with it or acquired- infection, injury, cancer |
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Phagocyte disorders/deficiencies |
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Definition
Effects (1) Innate immunity (non-specific) (2) Acquired- APC Chediak- Higaski Syndrome (no lysosomes) Chronic Granulomatous Disease (no H2O2 in macrophages) |
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Definition
susceptible to viral and intracellular parasites Addison’s disease: INNATE: Tc and adrenal gland (produces too much cortisol) Hodgkin’s disease: block T cell action kill APCs (can be acquired via a cancerous tissue attacking lymphoid) AIDs-ACQUIRED CD4 (Th) destroyed Di Georges: INNATE: born without a thymus (no T cells) Juvenile diabetes |
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Definition
susceptible to bacterial infections, especially skin and respiratory tract Bruton’s agammaglobulinemia |
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Combined immunodeficiency |
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Definition
SCID (severe combined immunodeficiency): INNATE: receptors on t cells can’t communicate with WBCs because of mutation at IL2 receptors (cytokine) (1) T cells can’t grow and divide (2) NO IMMUNITY |
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Transplant/graft rejections |
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Definition
MHC’s elicit t-cell response Autograft: self Isograft: twin Allograft: same species Xenograft: different species |
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Definition
study and use of antibodies in lab, clinic |
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Term
1975 Jerne, Milstein & Kohler |
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Definition
Goal: immortal B cell that would secrete 1 antibody Myeloma (cancer cell) + B cell -> hybridoma If the b cell was pre-exposed to an antigen then the hybridoma= MONOCLONAL AB PRODUCTION (MABs) |
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Definition
Western blot: electrophorize proteins and use an MAB to target a protein then use an anti-AB to target the original AB plus an enzyme to “mark/color” the AB. DNA: Southern blot Home Pregnancy Test: measures gomadotrophin hormone (MAB) Elisa: enzyme linked immunoassays If you have antibodies circulating in your body against an antigen, you are Sero + |
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