Micro Exam #1 2001 - J/‘ 1 £0 MEDICAL MICROBIOLOGY AND...

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Unformatted text preview: J/‘ 1. £0 MEDICAL MICROBIOLOGY AND ININIUNOLOGY EXAlVIINATION I AUGUST 31, 2001 T, g 7 0 fi «’37 ONE BEST ANSWER ONLY In cases when the immune system fails to localize an infection and bacteria invade the bloodstream (sepsis), very serious and potentially fatal effects may occur. Some of these effects include generalizedlamdilation leading to loss of plasma volume and shock, disseminated intravascular coagulation, and organ failure. What is the main mechanism responsible for these effects? ”WW A. Bacteria cause damage to endothelial cells and colonize different organs, such a lungs and liver, causing their failure. ® Systemic overproduction of tumor necrosis factor-0t (TNFa) and other pro—inflammatory cytokines results in vascular and metabolic alterations. C Systemic activation of lymphocytes due to overproduction of interferon-y (IFNy) leads to an autoimmune reaction against endothelial cells. D. Bacteria cause an overproduction of interleukin-10 (IL-10), leading to increased susceptibility to infection. E. Systemic activation of Th1 cells and release of lymphotoxin, which is toxic to other cells. Severe allergies and asthma are usually associated with an 0W cells and increased production of a cytokine that induces B lymphocytes to switch immunoglobulin class and produgelgE antibodies. In fact, inhibitors for this cytSEn—e might be useful in the therapy of allergic conditions. Which cytokine is this? Interferon-y ([FNy) Interleukin-l (IL—1) Tumor necrosis factor-a (TNFa) Interleukin-4 (IL—4) Transforming growth factor-B (TGFB) [email protected]? During a trip exploring the jungle forests of a Caribbean nation, you come across a plant extract that the locals claim to “cure” ,hcumallgid arthritis and other diseases of autoimmune origin. After purification, you discover that the extract has an active compound that ivnhflaitswthgprcggggtion of interleukin-2 @153). by activated lymphocytes. Based on this information, what would be the most likely effect of such compound and the probable basis of its immunomodulatory properties? J 71,341 ’4, [of (J A. Inhibition of the production of pro-inflammatory cytokines by monocytes. B. Decreased activation of neutrophils. /o.—[email protected] Inhibition ofT lymphocyte proliferation. D. Decreased production of leukocytes by the bone marrow. E Decreased expression of MHC class I and II expression by antigen-presenting cells. .. Q . How 15 the alternative pathway fer complement activation restricted to pathogenic (activating) surfaces and prevented from actuating on normal tissue {non-activating) surfaces? ,2: ' 22:” Antigenic surfaces stimulate factor D cleavage of factor B, forming the Bb fragment that binds to C3(HZO) and forms a stable C3-convertase. C3b is specifically deposited onto pathogenic surfaces by the action of properdin that binds only to pathogenic surfaces and not to normal tissue surfaces. C3b that is randomly deposited onto normal tissue is selectively destroyed, while C3b deposited onto pathogenic surfaces is allowed to form a C3-convertase. Specific sugars such as mannan or N-acetyl-D-glucosamine on bacteria are recognized by factors B and D, activating the alternative pathway selectively on pathogenic cell surfaces. Factor I initiates the alternative pathway selectively on pathogenic surfaces but its action is blocked on normal tissue. 5. Over a 5-year period, a prostitute is admitted to the hospital for 4 episodes of disseminated (systemic) infection with When Which laboratory tests should be ordered to rule out a possible immunodeficiency disease? .A. @ C. D. E. Tests for IgG subclass deficiency, especially IgG deficiency Tests for absence of one of the terminal components of complement forming the membrane attack complex (C5, C6 c7, or cs)/ 1.7 #322,}. x 222 , ,, 2 2,222. Tests for deficiency of components of the classical pathway(e/ (:{élw 1, C4, C2)~S¢ 5- Tests for B and T cell function to rule out a case of acquired common variable immunodeficiency (CVID) Tests for a selective deficiency of B cells making IgE antibody to Neisseria gonorrhea 1113222 a ,2 2 122,122,” it 22/22/22 222/: fig )3: How many different enzymes are involved in activation of the clmmafiiyyannfmplemcnt? 6-1—2- I @00qu )6 How does the trimolecular protein complex C5b,C6,C7 acquire the ability to insert into. lipid membfies? .2® “é Proteolytic cleavage of C7 exposes a lipid-binding site that promotes insertion of the complex into membranes. , A major conformational change exposes hydrophobic residues that are normally hidden, causing the complex to become lipophilic and insert into membranes. The lipid-rich S—protein binds to C5b-7, promoting its ability to insert into lipid membranes. Proteolysis of C5 into C5b exposes a lipophilic region of CSb, and this is stabilized by CSb complex formation with C6 and C7. Proteolysis of C8 catalyzes a conformational change in C5 and C6 that promote membrane insertion of the entire C5b,C6,C7 complex. ‘ a 4 -0 What 1s the mechanism thought to initiate cowation 1n the brains of patients with Alzheimer’ s I) disease. F: lifts”? £91155”? aim" IgM autoantibodies to myelin are present at increased levels in cerebral-spinal fluid and can be shown to readily activate the classical pathway in vitro with purified human myelin. Patients treated with a new generation of complement inhibitory drugs have shown a complete reversal ‘ in symptoms of dementia. A loss of complement regulatory proteins in the brain, especially DAF and MCP, leads to spontaneous activation of the altemative_p_athway 1n brain tissues Aging of brain tissue leads to exposure of AB peptide, neurofibrillary tangles, and DNA that bind Clq and activate the classical Wpathway of complement. Inflammatory cytokines trigger the release of proteolytic enzymes that cleave C3 and lead to activation of the alternative pathway of complement. ch specific tests for complement activation are useful in the diagnosis of panents with rheumatoid arthritis? 1"? a“: n9 {ape/AX if? ”’41"? m:w Assays for serum complement activation are of no value 1n the diagnosis of rheumatoid arthritis Patients with rheumatoid arthritis have elevate {serum levelsnf the Ba fragment of factor B that are diagnostic for this disease. a301M) «Coma» .j Autoantibodies to Type [I collagen 1n the seraflojgpatients with rheumatoid arthritis generate immune complexes' 1n sermn that are heavily coated with C3d. Most patients with rheumatoid arthritis have elevated serum levels of C3a, 04a, and C5a that are sensitive and specific diagnostic feature. Serum levels of C3 and C4 are frequently reduced to <10% of the normal range. 10. What is the major reason for the failure of tumor twang/”therapy protocols in patients with metastatic cancer despite their initial success in generating tumor-specific cytotoxic T cells (CTL)? A. Metastatic tumors become resistant to the cytotoxic effector mechanisms of CTL. )3”. Mutant CTL that no longer express tumor-antigen specific T cell receptors develop in patients with metastatic cancer. C. Rapidly dividing metastatic tumors outnurnber the total size of the Specific CTL pool that can be generated in most patients. D. Cytotoxic drug resistant tumor cells develop during the metastatic disease process that are specifically resistant to CTL. ® CTL select a mutant tumor clone for survival that no longer expresses MHC class I molecules. 1 1. Why does the binding of iC3b to a tumor cell not result 1n opsonization for killing by macrophages or neutrOphils in the same way as would occur with iC3bW bound onto a bacterium or yeast? A. Tumors are resistant to complement activation and take up much less iC3b than do microorganisms. B. The iC3b attached to tumor cells is rapidly destroyed by proteolytic enzymes that are secreted by the tumor. C. Tumor cells secrete IL—10 and TGF-B that suppress the cytotoxic function of macrophage and neutrophil _ CR3 and CR4. @ Tumors lack microbial polysaccharides such as fi-glucan that must bind to CR3 in combination with iC 3b in order for killing to be triggered. E. Bacterial and yeast surfaces present clusters of iC3b acceptor sites that are not found on tumor cells and which are necessary to activate CR1 or CR2 for cytotoxicity. 1 l 12. What are some of the advantages in using a tumor immunotherapy protocol based on tumor-specific antibodies ’ rather than on cytotoxic T cells? Tumor cells must express only MHC class II molecules and do not have to express MHC class I molecules. Molecularly engineered monoclonal antibodies are functional in patients who are immunosuppressed or whose tumor cells no longer express MHC class I molecules. Vi! Antibody based therapies are always ineffective in producing tumor remission, providing few, if any, advantages over T cell-based immunotherapy. Antibodies can elicit multiple effector mechanisms to kill tumor cells, especially complement mediated killing by the membrane attack complex and C3-dependent opsonization. ‘ Antibody-mediated killing of tumor cells is usually more effective than T cell-mediated cytotoxicity of tumors . 11 @ 1117-561 1: 13. Which function(s) of complement is (are) missing in patients with a genetic deficiency of C6? Opsonization of bacteria via the alternative pathway Killing of Gram negative bacteria ~14 3 g, 1:1 Inflammation and chemotaxis of macrophages and neutrophils Solubilization and clearance of immune complexes £8357/fl C, / 11,? Generation of immunologic memory and isotype switching from IgM to lgG hcohe 14. A 37 vear old _Cauc_asian female presented in the emergency room with painful swelling of the hands, facial rash, and problems with breathing. The alert intern who had recently reviewed his clinical immunology noteie immediately suspected a previously undiagnosed case of heredity gngigegwigfiéli) and ordered tests for C1- inhibitor, C3 and C4 Although the senior resident approved these tests, she ordered additional tests for 1 antinuclear antibodies and double- -strande_dwl;)‘le. Not only did all of the tests ordered by the intern reveal abnormal results but also the results of tests ordered by the senior residegtwgrgpositive Based on these physical symptoms and laboratory tests only, what 13 the most likely diagnosis? 41.1 L111, C, (11 "“9 .i (19 Systemic lupus erythematosus (SLE) \j" B. Hereditary angioedema (HAE) w 1 _1( . C. Rheumatoid arthritis (RA) b A“ 3 r" ”L A [9 D. Asthma associated with allergic dermatitis 0 5 ION/3 E. HAE associated with asthma J {3.) Why is a hereditary deficiency of mflninflrrdinglgtinlflm more likely to lead to problems with yeast infection in children than in adults? A The neutrophils and macrophages of children require MBL for recognition of yeast, whereas adult phagocytic cells have higher surface densities of CR3 and CR4 that can serve this function ’ B , Adults develop antibodies to yeast that activate the classical pathway, reducing the need for MBL and the lectin pathway of complement activation fl Children are more dependent upon the lectin pathway because the alternative pathway has a reduced capacity to recognize yeast as the result of higher serum levels of factor H and factor 1 than are found In - adults. /B’./ Children are much more likely to be exposed to yeast infections than are adults because of infrequently changed wet diapers that lead to candidiasis E. Adults develOp higher serum levels of properdin that serve to promote activation of the alternative pathway of complement and reduce the need for MBL and the lectin pathway of complement. 16. 17. 18. 19. 20. Which one of the following autoimmune conditions is treatable in newborn children born to a mother with one of the following conditions by I’WS for removal of the antibody? It is an example of aEWthy acting 3; argcsptornntagnnist of the acewlcholingregentor to prevent the bWWm wan-smru and blocking the transmission of normal neuronal impulse, ultimately resulting in muscle weakness. Grave’s disease insulin dependent diabetes mellitus (IDDM) Hashimoto’s thyroiditis {29 myasthenia gravis B. C. D. E. systemic lupus erythematosus (SLE). A patient with acute rhgurnatoidanhritis feels systemically ill with a low gr_a_de fever, malaise, morning stiffness, and fatigue. The protein(s) and/or cytokine(s) most likely to be responsible for these symptoms are: W /!C Rheumatoid factor @ IL 1 and TNF : L... " t a C. 1-.L4E3J1dILlOI-TYga ’ D. C 1-C9 E. IgG mwfim—qn‘ Which one of the following is mediated by antibody directed against thyroglobulin? ,fi"”‘ a s” Graves‘ Diseasew; :4 ‘ 1- ‘c-eggmitf"W ’ “in” myasthenia gravis rheumatoid arthritis :3...) Hashimoto‘s Disease ‘ ' B. ‘ C. D. E. systemic lupus erythematosus Which one of the following best describes a transglantationmey from an individual 1195;;ng the recipient? Additional hint; this person needed trip‘leirnmungsuppmggssive therapy following surgery for the rest ofhis life: A. xenograft " ’i , , .. 3- Syngrafi- '“mvlfje§\lt iéin‘etem @ allograft bi“ ‘acfltafa'fi ’97 autograft tyrerteani- ’5: photograft Which one of the following immunosuppressive agents, which i s structurally a egglic peptide inhibits the cytoplasmic activation of T cells during resWell cycle, by blocking the phosphatase activity of M _ , calcmeurin? It resembles cyclosponn in its mode of action. _.__..._.. azathioprine Q! AMEW Efimflfli— EwflwL‘h‘av‘ cyclophosphamide corticosteroids A. B. C. D. anti-tac antibody , ' @ tacrolimus (FK506). «sincewriiwias E) 33"4, "35—4.? {44st 3F, Which one of the following applies to hyperacute rejection? 6) onset within minutes to hours 34.4 ,5 4? 5 VK‘Z’W‘A 7 WM flBf generally causes a slow progressive tissue damage ,fi.’ onset within months to years . (“rattan ET treatable with antilymphocyte serum — cm *5; E. primarily due to T cell activation My”); 22. Most, if not all, antibody preparations currently in clinical use are “monoclonal” antibodies. What are “monoclonal” antibodies? 0...“...— 4 All antibody molecules in the preparation have the same specificity, although idiotype may vary. #3:.) All antibody molecules in the preparation have the same specificity, the same isotlpe, and the same V idiotvpe. C All antibody molecules in the preparation were derived from an immune response elicited by injection of one single antigen molecule. /DC All monoclonal antibodies react with lymphocyte membrane molecules which are assigned a “CD” number. E. All monoclonal antibodies have a variable region (VDJ exons) that was “captured” from a single tumor cell. \23) A young physician discovers that his roommate has nevegbeen immunized to tetanus. To correct this oversight " he injects the recommended quantity of tetanus toxoid intradermally. Which of the following is the earliest event to occur at the site of injection? “MM“ r\ . . . . LA/r/ an increase in vascular permeability. B. appearance of E-selectin on the vascular endothelial cells. /€./ diapedesis of neutrophils. /D’. diapedesis of lymphocytes. E production of TNF-a. 24. Which of the following cytokines would contribute to the Wonk at the site of immunization? @ IL—l. B. IL-2. C. IL-3. D. lL—4. E. IL«5. 25. Which of the following cells would be the first $9.919???“ into the inflamfigydiissue? A T lymphocyte. B lymphocyte. Monocyte. B. C. ® Neutrophil. E. Mast cell. 26. Which cell is the major producer of IL-1 in an aggtejgflWse? A. T lymphocyte. B lymphocyte. Monocyte/macrophage. ,BT Neutrophil. /E’f Mast cell. 27. Which class of antibody will be the first to appear in the serum of the roommate after immunization with tgtgnps toxoid‘? IgA. lgD. IgE. IgG. IgM. @UOW? 28. A few months later the physician injects tetanus tgzoid intradermally into his roommate a second time. What is the dominant class of antibody that would be produced? A IgA. xB’. IgD. C. IgE. @ IgGé- ,8? IgM. 29. The antibody is produced by plasma cells. The majority of the plasma cells producing antibody in response to the tetanus toxoid booster are located in the lymph nodes draining the site of injection. B. in the spleen. C. in the blood. D. in the liver. E. at the site of inflammation caused by the intradermal injection. 30. The physician obtains a blood specimen from his roommate and confirms that the serum contains an impressive concentration of antibody. What lab test would provide arquantitative measure of the concentration of anti-tetanus toggid antibodies in the serum? ’ A. Flow cytometry. ELISA. C. Agglutination. D. Western blot. E. Nitroblue tetrazolium. A. (E) 9:» E. Unable to suppress his urge to play scientist, the physician injects itimes the normal amount of tetanus toxoid intradennally into his roommate one month after the second in jection to investigate whether he can further increase the anti-tetanus antibody concentration in his roommate’s serum. That night his roommate complains of pain in his arm and the physician notes that the site of injection has discolored to a red-brown, suggesting . m - . . . M microhemorr hage. What is the likely cause of this reaction? / Prausner-Kustner reached-ET! [31/ " =.t,~é§;jé 454% % Late-phase reaction. tr- (1 v Arthus reaction.~7‘fl‘_~.§du II (My ., . ., 3, § _ UWMk/W (”.IXIJZ'i‘ 'hoen . Granulomatous reaction. 3 I d M' flair/4“ 6k i le“ D la ed eh e ‘ ' ' _ e y typ yp rsensrtmty MW “MS a?” c minMarrkw 32. In an attempt to confirm the mechanism of the reaction, the student biopsies the afflicted tissue and identifies the cell type that dominates the inflammatory £5211 infiltrate. Which cell type would dominate the late phase response of a type I hypersensitivity reaction? A. @ C. D. E. neutrophils. 4"? ffi 3' “l i“ 93‘ eosinophils. monocytes/macrophages. Th1 cells. -~ 3;???" B cells. 33. Which cell type would dominate the inflafnnnétolinflltrate of a granulomatous reaction? A. B. © D. E. neutrophils. eosinophils. monocytes/macrophages. T112 cells. B cells. 34. Which cell type would dominate the inflammatogy infiltrate of anArthus reaction? (A; neutrophils. B. eosinophils. C. monocytes/macrophages. D Th1 cells. E B cells. 35. A major mediator of Arthus reactions is "_~'—--- - A. IL«2. B. IgE. ,8.’ eotaxin. D. prostaglandin. ® C3a/C5a anaphylatoxin. 36. ' Negative selection of T cells during intrathymic development is an example of: A. anergy clonal deletion. C. , split tolerance. D. immune deviation. E. cytokine antagonism. 37. The tendency of Th cells to polag‘ze to either Th1 or Th2 cells results in polarization of the immune system, a phenomenon that is referred to as: A anergy B.‘ clonal deletion. © split tolerance. D. immune deviationfgmw 5/.” E. cytokine antagonism. if 38. Th1 cells inhibit the development of Th2 cells by: A. anergy B. clonal deletion. C. split tolerance. D. immune deviation. ® cytokine antagonism. 39. CW kill virus infected cells by: A. Releasing peroxides and nitric oxide. B. Releasing chemokines. C. Releasing interferons. ® Releasing perforin and granzymes. E. Polymerizing C9. 40. Natural Killer cells will W1 if: the tissue cell displays CD40 on its membrane. the tissue cell displays viral DNA encoding for CD40-like molecules. the tissue cell displays viral peptides presented on class I MHC molecules. the tissue cell displays mutated or abnormal proteins on its membrane. 096%?" Y‘ 3. ,, tibod sing a receptor specific for: $5 the tissue cell displays too little class I MHC to engage the NK Inhibitory Receptor. ’ B. C. D. E. 41. In ADCC reactions, NK cgus can bind to, and kill, cells coated wi r- 1. A. Peptides presented on MHC class I. B. y Peptides presented on MHC class II C. A carbohydrate of glycolipids/glycoproteins present on all cells. (Q Fc domains of IgG. ' B. Virus proteins. Items 42. - 45. @D 43. 45. A patient suffering from recurrent skin infections is referred to you by a colleague with the suggested diagnosis of Chronic Granulomatous Disease. What function is defective in Chronic Granulomatous Disease? ,X Diapedesis is reduced due to an integrin defect.’ L0” Oxidative burst is reduced due to an oxidase defectw Phagocytosis is reduced due to abnormal f...
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