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Final Study Guide

by: Dakotarae Sloniker

Final Study Guide 5354

Dakotarae Sloniker
GPA 3.1

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About this Document

A review of what we went over in class and what Professor Rycher said would be on the final exam.
Introduction to Microbiolgy
Professor Rychart
Study Guide
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This 18 page Study Guide was uploaded by Dakotarae Sloniker on Friday August 19, 2016. The Study Guide belongs to 5354 at Boise State University taught by Professor Rychart in Spring 2016. Since its upload, it has received 8 views. For similar materials see Introduction to Microbiolgy in Microbiology at Boise State University.


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Date Created: 08/19/16
Microbiology final 2016 Study Guide  I. Nonspecific Defenses A. Not specialized to a particular bacteria B. General for any kind of pathogen C. Two levels 1. Barriers a) Skin  (1) Sweat glands produce oily acids that inhibit pathogens  (2) pH,  (3) unsaturated fatty  acids,  b) Mucous membranes  (1) Line the intestines,  respiratory system, and genitourinary system (2) Produce saliva, tears,  nasal secretions, etc.  (a) Lysoso mes are produced in these secretion they digest cell  walls of bacteria  (b) Produc e toxic oxygen products such as peroxide , nitric  oxide, and hydroxyl that help in the breakdown of  microorganisms (3) Mucous traps  membranes.  c) Cilia (1) Small hairs lining  respiratory system that beat away from the lungs and move  the mucous and trapped particles out of the body   d) Gastric Juice  (1) Concentrated HCl and protease that destroy pathogens in the stomach 2. Internal defenses a) Leukocytes ­ white blood cells  (1) Phagocytes (a) Cell  eaters  (b) Most  important  (i) B asophils (ii) E osinophils (iii) N eutrophils (iv) M ast cells (v) M onocytes (vi) M acrophages (a) B ig eaters  (b) A moeba (c) M ost famous/not most abundant  (2) Lymphocytes (a) Specifi c defense mechanism  (3) Natural Killer Cells  *NK cells (a) Differe nt from phagocytes  (b) Identifi es virus infected cells and some tumor cells  (c) Lyses  (split open) cells and attacks cell walls  3. Inflammatory Response a) Tissues are injured by bacteria,  trauma, toxins, heat, etc. b) Damaged cells produce histamine,  bradykinin, and prostaglandins and they cause blood vessels to  leak and swell the tissue, isolating foreign particles.  c) Chemicals attract white blood cells  and they eat the bad stuff in phagocytosis.  d) Responds to antigens and destroys  the substance e) Complement  (1) 30 proteins C1­C9 (2) Enhances the abilities  of antibodies and phagocytic cells to rid body of pathogens  (innate immune system) (3) Liver synthesized by  liver, that are normally inactive  (4) It amplifies a normal  immune response  (a) One  reaction activates another (i) C lassical Pathway (a) A ntibodies attach to antigens and this  body binds to C1 (b) C 1 activates C2 and C4 by splitting  them into C2a and C2b and C4a and  C4b. (c) C 2a+C4b= C3 (d) C 3 ­> C3a and C3b, a participates in  inflammation and b reacts in  cytolysis and opsonization (ii) A lternate Pathway (a) D oes not involve antibodies (b) C 3 is always in the blood combines  with compliment protein factors B, D and P on microbe surface.  (c) C 3 splits to a and b and triggers  inflammation response   (b) Opsoni zation ­ enhances phagocytosis of antigens C3b has  most important opsonizing activity.  4. Antigen­Antibody reaction that initiates immune  response.   5. Interferons (glycoproteins produced by virus­ infected cells):   a) alpha  (1) Interferes with virus  multiplication (2) Host cell specific  (3) Trick the host cell  into creating antiviral proteins  (a) Ogilod enylase synthetase  (b) Protein kinase  b) Beta (1) Interferes with virus  multiplication (2) Host cell  (a) Ogilod enylase synthetase  (b) Protein kinase  c) Gamma­ interferon activates  neutrophils and macrophages among other things. (1) Produced by  lymphocytes  (2) Induces neutrophils  and macrophages   (a) Macro phages inhibit ATP production and produce nitric  oxide (b) Also  increase antigen production  d) Species specific  (1) Animal cells  II. Specific Defenses A. B cells and T cells stem from stem cells in bone marrow B. Blood and lymphoid organs C. Target insides of cells  D. Best at fighting viruses  E. Epitopes 1. Is the specific piece the antigen binds to when the  antibody binds 2. Determinants ­ determines the antibody that  attaches F. B cells (humoral response):  1. viruses 2. bacteria,  3. Toxins cells  G. T cells (cellular response): come from Thymus gland 1. Antigenic­ t cells bind directly to the antigenic  peptide of MHC molecules  2. Have receptors  3. T Helper cells coordinate with B cells in producing  antigens  4. T cytotoxic cells   a) Kill virus infected cells and tumor  cells, cause a anergic state that prevents autoimmune disease.  b) Are what is behind organ transplant  rejection 5. T­lymphocytes 6. Cell mediated immunity  7. Do not bind to antigens but sense the presence of   Antigens  III. Clonal selection A. Explains the function of cells, lymphocytes, in the immune system B. B cells are pre existing and a specific antigen produces a specific B cell response to produce a specific antibody.  C. Explains the diversity in antibody specificity 1. IgG ­ main antibody found in the blood and  extracellular fluid a) 80% of antibodies  b) Controls infection with tissues  c) Binds to viruses, bacteria, and fungi  d) Binding to cause immobilization e) Coating pathogen surfaces f) Activates the classical pathway and  causes pathogen elimination 2. IgM a) 6% of antibodies  b) Stay in blood vessels  c) Produced by B cells d) Largest antibody  e) In the spleen f) Does Not diffuse well and is found  in low quantities  g) Found in serum h) Contributes to opsonization i) Causes C3b to bind to an antigen  3. IgA a) 13% of antibodies  b) 15 grams secreted from the intestines c) Plays a role in mucous membranes d) Produced in mucous lightings  e) Tears, saliva, sweat, colostrum and  secretions in the  genitourinary tract, and respiratory epithelium  4. IgD a) .02% of antibodes b)  In blood, lymph, and the tops of B  cells Plasma membranes c)  In immature B lymphocytes  d) In blood serum  e) In species from fish to humans,  except birds  f) Signals B cells to activate, like IgM  cells g) Binds to basophils and mast cells to  activate them  5. IgE a) .002% of antibodies  b) Allergies and cause an allergic  reaction c) In the nose, lungs, and throat d) Asthma, sinusitis, allergic rhinitis  e) Chronic urticaria f) Atopic dermatitis  g) Anaphylactic drugs, bee stings,  antigens in immunotherapy   D. T C D8+ bind to MHC class I),  1. Binds to degradation cytosolic proteins  2. Sent into the ER of the cell  3. Shows Tc cells CD8 receptor what molecules to  bind to  4. Binds to MHC class 1 E. T H D4+ bind to MHC class II),    1. Occurs by phagocytosis  2. Extracellular proteins are endocytosed and digested  in lysosomes and fragments are loaded on MHC class 2 molecules prior to cell surface migration  3. Derived from extracellular proteins (ENDO) F. T REG (TS) 1. 5­10% of T cell population  2. Sub of CD4+ 3. Combat autoimmunity by suppressing T cells that  escape deletion   4. Helps avoid the body reacting against itself  5. Keeps the bacteria needed for digestion from being  removed and protects the fetus from rejection G. T H produce activating cellular immunity 1. Produce cytokines and interferon gamma particle  2. Activate cells active in cellular immunity  3. Stimulate production of antibodies  4. Enhances complement and opsonization and  inflammation   5. Help fight against bacteria and protozoa  6.  and antibody production with respect to  complement (opsonization and inflammation)). H. T H  1. Also produce cytokines but the ones associated with production of antibodies  2. IgE 3. Activates eosinophils against infection by parasites  I. Antigen presenting cells:  1. macrophages and  a) Large white blood cell b) Digests (1) Cellular debris (2) Foreign substances (3) Microbes (4) Cancer cells (5) Anything that does  not have a specific protein on its surface (healthy body  specific proteins)  2. dendritic cells a) Antigen presenting cells b) Mammalian immune system c) Process antigens material and present it on the surface so the T cells can find it d) Bridge between innate and adaptive  immunity  e) In tissues that come in contact with  external environment f) Inner lining of the lungs,nose,  stomach and intestines   g) Interact with T and B cells in lymphs J. NK cells 1. Natural killer cells are cytotoxic lymphocytes  2. Innate immune system 3. Rapid response to viral infection ­ 3 days and  respond to tumor formation  4. Detect MHC on infected cell that triggers cytokine  release and apoptosis or lysis of the infected cell then occurs  5. Analogous to cytotoxic T Cells  K. Cytokines:  1. IL­1,  a) 11 cytokines that regulate immune  and inflammatory response to infection  b) Induces a complex proinflammatory  cytokines  c) Discovered first  and have a strong  proinflammatory response 2. IL­2 a) Signaling molecules regulate white  blood cells  b) Responsible for immunity c) And is responsible for bodies natural  response to microbial infection  d) Discriminates between self and  nonself proteins  3. IL­12 a) Close with natural killer cells b) Enhances cytotoxic activities c) Produced by dendritic cells,  macrophages and neutrophils and human B­lymphoblastoid cells  d) Response to antigenic stimulation e) Differentiated T cells f) Stimulates growth and function in T  cells g) Stimulates gamma interferon  production from NK cells and reduces IL­4 suppression of  interferon gamma  4. others Cytokine Cytokine Cytokine Cytokine Cytokine Cytokine Receptor Source Targets Main Function Disease  Association IL­1α; IL1RI and Macropha Macropha Inflammatory; ↑ = IL­1b IL1R­AcP ges, many ges, promotes inflammatory others thymocyt activation, bone es,   CNS, costimulation, and resorption; others secretion   of gout; promotes cytokines   and Th17 response other   acute­phase proteins; pyrogenic IL­1ra Soluble     IL­1ra   and   the   (antagonis decoyrece soluble   decoy t) ptor:IL1R receptor   complex II  and inhibit   IL­1­ IL1R­AcP mediated inflammatory responses IL­2 IL2Rα, T cells T, B, NK Proliferation; ↓ = IL2Rb, cells,   andenhancement   of lymphoprolifer and macropha cytotoxicity, IFNγ ative disease IL2Rγ ges secretion,   and and antibody susceptibility production to autoimmune disease; reduced Treg development. ↑ = reduced Th17 development. IL­3 IL3Rα T   cells, Hematopo Differentiation and  and mast ietic survival   of IL3Rb cells, progenitor lymphoid   and eosinophil s,   macro­ myeloid s phages, compartment mast cells IL­4 IL4Rα T   cells, T cells, B Proliferation; ↓ = and mast cells cells, differentiation   ofusceptibility IL2Rγ  or macropha Th2; promotes IgG to IL4Rα ges, and   IgE extracellular and monocyte production; pathogens and IL13Ra1,I s inhibits   cell­ L13Ra2 mediated decreased immunity   and response to Th17 development allergens. ↑ = allergic asthma. IL­5 IL5Rα Th2 cells Eosinophi Proliferation   and ↓ = and ls, B cells activation; eosinophil and IL3Rb hallmark   of   Th2B-1 cell effector cells deficiency. ↑ = allergic asthma. IL­6 IL6Rα Macropha Wide Inflammatory   and ↓ = deficient and ges,   T variety of costimulatory innate gp130 cells, cells:   B action;   induces immunity and fibroblast cells,   T proliferation   and acute- phase s,   and cells, differentiation; responses, others thymocyt synergizes   with lymphopenia es, TGFb   to   drive myeloid Th17 cells, osteoclast s IL­7 IL7Rα Thymic B cells, T Homeostasis, ↓ = severe and stromal cells, differentia­   tion,combined IL2Rγ cells, thymocyt and survival immune bone es deficiency marrow, (SCID) and spleen IL­9 IL9R  and T   cells T   cells, Proliferation;   IL2Rγ (Th2) mast promotes   Th2 cells, cytokine secretion neutrophil s, epithelial cells IL­10 IL10R1 Differenti Macropha Immune ↓ = immune and ated   T ges,   T suppression; pathology due IL10R2 helper cells, decreases   antigen to uncon- cells, dendritic presentation   and trolled Tregs,   B cells,   B MHC   class   II inflammation. ↑ = inhibits cells, cells expression   of dendritic dendritic   cells; sterile cells, down­   regulates immunity to others pathogenic   Th1, some Th2,   and   Th17 pathogens. responses IL­11 IL11Rα Stromal Hematopo Proliferation ↑ = and cells ietic stem exacerbates gp130 cells,   B airway cells, diseases megakary ocytes IL­12 IL12Rb1 Macropha T   cells, Differentiation and ↓ = impaired (p35  + andIL12R ges, NK cells proliferation; Th1 responses p40) b2 dendritic promotes Th1 and and increased cells,   B cytotoxicity susceptibility to intracellular cells, neutrophil pathogens s IL­13 IL13Ra1,I T cells B   cells, Goblet   cell ↓ = impaired Th2 responses L13Ra2 macro­ activation in lung and phages, and   gut; to extracel- IL4Rα others proliferation   and lular promotion  of IgE pathogens production; and allergens. ↑ = regulation of cell­ exacerbates mediated immunity airway diseases. IL­14 Not T cells B cells Promotion   of   B   defined cell growth IL­15 IL15Rα, Broad T   cells, Proliferation   and ↓ = IL2Rb, expressio NK   cells, survival;   cytokinedeficiency in and n   in epithelial production NK cells and IL2Rγ hematopo cells, defective ietic cells others generation of memory T cells IL­16 Not T   cells, CD4+   T Recruitment   of   defined eosinophil cells CD4+ T cells s,   mast cells IL­17A IL17RA Th17 Mucosal Proinflammatory; ↓ = or cells   and tissues, protective susceptibility IL17RC others epithelial immunity in lung; to and tight   junction extracellular endothelia integrity; promotes pathogens ↑ = exacerbates l cells mobilization   of neutrophils   and organ- specific cytokine autoimmune production   by inflammation epithelial   cells; promotes angiogenesis IL­17B   Intestine       and pancreas IL­ 17C   thymus       and spleen IL­17D   T   cells,       smooth muscle cells, epithelial cells IL­17F IL17RA Th17 Mucosal Similar function as Not well or cells tissues, IL­17A but with 2 defined. ↑ = IL17RC epithelial logs lower receptor increases neutrophil and affinity endothelia recruit- ment l cells at high concentration. IL­18 IL18R Macropha Th1 cells, Proinflammatory; ↓ = impairs and  IL18­ ges, NK   cells, induction of IFNγ Th1 responses R­AcP others B cells IL­19 IL20R1 Monocyte Keratinoc Proinflammatory ↑ = psoriasis and s, others ytes, other IL20R2 tissues IL­20 IL20R1 Monocyte Keratinoc Proinflammatory ↑ = psoriasis or s, others ytes, other IL22R1 tissues and IL20R2 IL­21 IL21R Differenti T cells, B Proliferation of T   and ated   T cells,   NK cells;   promotes IL2Rγ helper cells, differentia­ tion of cells (Th2 dendritic B   cells   and   NK and Th17 cells cytotoxicity subsets) IL­22 IL22R1 Th1   and Fibroblast Inflammatory, ↑ = psoriasis and Th17 s, antimicrobial IL10R2;I cells,   NK epithelial L22BP cells cells IL­23 IL23R Macropha T cells Inflammatory; ↓ = (p19   + and ges   and promotes susceptibility p40) IL12Rb1 dendritic proliferation   of to extracellular cells Th17 cells pathogens. ↑ = exacerbates organ- specific autoimmune inflammation.   IL­24 IL20R1, Monocyte Keratinoc ↑ = antitumor IL22R1, s,   CD4+ ytes effects IL20R2 T cells IL­25 (IL­ IL17RB Th2 cells, Non-B, Promotes   Th2 ↓ = impairs 17E) mast cells non-T, differentiation and Th2 responses cKit+, proliferation to FcεR− extracellular cells pathogens such as worms IL­26 IL22R1 Activated       and T cells IL10R2 IL­27 WSX­1 Activated T   cells, Induction of early ↓ = immune (p28  + and dendritic others Th1 differentiation pathology due to EBI3) gp130 cells by   stimulating expression   of   thencontrolled Tbet transcrip­ tioninflamma- factor;   Inhibitiontory response of   effector   Th17 cel   responses   by inducing STAT­1­ dependent blockade of IL­17 production IL­ IL28R1 Activated   May   promote   28A/B/IL and subsets of antiviral responses 29 (IFNλ IL10R2 dendritic family) cells? IL­30           (p28 subunit ofIL­27) IL­31 IL31Rα Activated Myeloid Proinflammatory ↑ = atopic and T cells progenitor dermatitis; OSM­Rβ s,   lung allergic epithelial asthma cells, keratinoc ytes IL­32       Induces   proinflammatory cytokine production IL­33 ST2   and Macropha Mast Costimulation, ↑ = atopic IL1R­AcP ges, cells, Th2 promotes   Th2 dermatitis, dendritic cells cytokine allergic asthma cells production IL­35   Tregs Effector T Immune   (p35  + cells suppression EBI3) L. Monoclonal antibodies (how are they produced?)  1. Made by identical immune cells 2. Clones of parent cells  M. Immunological memory:  1. The ability of the body to remember a certain  antigen and the pieces that  2. Allows more rapid response  3. protect it 4. primary response,  a) Is the adaptive immune response to  initial exposure of an antigen b) Also known as priming, generates  immunological memory  5. secondary response a) Memory response b) It can go to secondary, tertiary and  so on depending how many times you are exposed to that antigen  N. Active vs passive immunity etc., antiserum 1. Active a) Produced when it comes in contact  with antigen b) Not immediate c) Long lived d) Antibodies are produced 2. Passive a) Antibodies are obtained outside  b) Develops immediately  c) Few days lived d) Introduction of antiserum called  serum sickness, allergic reaction to a serum typically because of  medications with certain proteins , the liquid part of the blood that  produces antibodies helps prevent from poisonous substances  O. Serology: ELISA (direct and indirect),   1. Enzyme­linked immunosorbent assay  2. Fluorescent antibody a) Introduction of fluorescence helps  count the presence quality of antigen in wells 3. Agglutination a) Ultrasensitive solution phase that  detects antibodies  b) Antibodies bind to agglutinate and  synthetic antigen­DNA conjugates    4. complement fixation a) Immunological test that detects the  presence of specific antibody or specific antigen in a patient's  serum b) Diagnose infections  IV. Hypersensitivity A. Type I  anaphylaxis (local, systemic) 1. Immediate 2. Allergic reaction to a specific type of antigen  referred to as an allergen 3. Exposure can be ingestion, inhalation or injection 4. B cells are stimulated by CD4+TH2 cells to make  IgE, which make it a hypersensitivity reaction. 5. Minutes after exposure  a) Localized (1) Includes allergic  rhinitis, itchy watery eyes congestion coughing sneezing  short breath hives skin rash food allergies  b) Systemic (1) Counters epinephrine  injection B. Type II (cytotoxic) thrombocytopenic purpura  1. Antibodies in immune system bind to antigens on  cell surfaces 2. These can be intrinsic­self antigens or extrinsic­  absorbed during exposure  3. Cells are recognized by macrophages or dendritic  cells and causes B cell response to form antibodies  4. Grave’s disease a) Autoimmune disease that affects the  thyroid  b) Hyperthyroidism and enlarged  thyroid  c) Overactive production of thyroid  hormones d) Thyroid autoantibodies that activate  the thyroid stimulation hormone receptor stimulating synthesis  5. myasthenia gravis a) Neuromuscular disease that leads to  muscle weakness, circulating antibodies block acetylcholine  receptors that inhibits secretion and causes muscle weakness C. Type III (immune complex) glomerulonephritis 1. Accumulation Of immune complexes that have not  adequately cleared and it causes a rise in inflammatory response and  attraction of leukocytes  2. Progresses to a point of disease 3. Soluble antibodies unlike in type 2 4. lupus,  5. rheumatoid arthritis D. Type IV (celluar=delayed hypersensivity) contact dermatitis,  1. MS, Hashimoto’s thyroiditis,   2. Addison’s disease E. Many of the above are autoimmune diseases V. Vaccines A. Inactivated virus –  1. polio,  2. rabies,  3. influenza B. Attenuated virus –  1. Mumps,  2. measles,  3. rubella,  4. chickenpox,  5. Sabin (polio),  6. vaccinia C. Toxoid –  1. diphtheria,  2. tetanus D. Inactivated whole cells –  1. pertussis ,  2. typhoid E. Others: attenuated influenza, acellular fragments of Bordetella  pertussis F. Conjugated vaccine: Hib (polysaccharide from Hemophilus  influenzae G. Conjugated with protein). Also, meningitis vaccine H. HepB (antigenic fragments produced by recombinant technology)  Pneumococcal vaccine: polysaccharide from multiple strains of Streptococcus  pneumoniae.   I. DNA vaccines. VI. Ch 25 know tables on page 728 (Bacteria) and 740 (Protozoa) VII.  Ch 26  know table on page 767  


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