Micro Assessment 7 – Flashcards
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| 1. What family is the measles virus in? |
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| 1. Paramyxoviridae (morbillivirus genus) |
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| 2. Why is Measles considered a “new” virus? |
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| 2. No accounts in early Greek, Required population >100,000, Trade route opened avenue for transmission |
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| 3. What 3 viruses cause multi-system infections and humans are the only known host? |
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| 3. Measles, Mumps, Rubella |
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| 4. How is Measles different from other paramyxoviruses? |
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| 4. Lacks neuraminidase activity, has H protein instead of HN; Receptors are CD46 and SLAM; Forms intracellular inclusion bodies |
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| 5. What is a distinctive feature of cytopathology for Measles? |
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| 5. Intracellular inclusion Bodies |
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| 6. What is the Entry and Replication strategy for Measles? |
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| 6. 1. MV binds receptor (CD46, SLAM), 2. Binding activates F protein, causes membrane fusion (entry). 3. Replication and assembly similar to other negative-strand RNA viruses |
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| 7. Who typically is infected by Measles? |
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| 7. Children |
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| 8. How is Measles spread? |
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| 8. Respiratory route |
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| 9. What is the main cause of mortality from measles? |
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| 9. bacterial pneumonia |
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| 10. How long does the latent period of measles last? Are there symptoms? |
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| 10. 10-14 days; No |
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| 11. What are the symptoms following the latent period of measles? |
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| 11. 2-3 day prodrome of high fever (101-105), cough, conjunctivitis (Photophobia), rhinorrhea |
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| 12. What kind of rash develops after the initial symptoms? |
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| 12. maculopapular rash |
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| 13. What does the maculopapular rash of measles coincide with? |
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| 13. a strong cell-mediated immune respone and virus clearance |
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| 14. What viruses do not use sialic acid and don’t have neuraminidase? |
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| 14. Measles, RSV, Rhino (class clicker question) |
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| 15. What is the Clinical Case Definition of Measles? |
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| 15. 1. Rash >3 days, 2. Temperature >38.3C(101F), 3. Cough, rhinorrhea, and/or conjunctivitis. |
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| 16. When do cases of measles need to be reported? |
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| 16. If symptoms are epidemiologically linked to another confirmed case of measles. |
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| 17. Where is the initial site of measles infection? |
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| 17. Tracheal and bronchial epithelia |
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| 18. After 2-4 days how does measles spread to the lymph nodes? |
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| 18. carried by pulmonary macrophages |
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| 19. What are Warthin-Finkeldey cells? |
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| 19. Reticuloendothelial giant cells that are created by measles virus replicating in the lymphoid tissue |
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| 20. What does amplification of measles in the lymph nodes result in? |
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| 20. Viremia and infection of other tissues and organs |
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| 21. What are the primary cells infected by measles in the blood? |
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| 21. Monocytes (other major cell types – epithelial, endothelial, macrophages) |
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| 22. When is the patient with measles infectious? |
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| 22. 1-2 days before symptoms of viremia occur (Rash and Koplik spots) |
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| 23. How long after exposure to measles is a person infectious? |
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| 23. 10-20 days |
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| 24. Where can measles be cultured? |
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| 24. mucous membranes of nasopharynx, conjunctivia, mouth, and blood |
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| 25. What are small red spots with blue-white center found in upper lip and cheek called? |
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| 25. Koplik spots |
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| 26. How does the Maculopapular Measles rash spread? |
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| 26. Starts on the back of the neck or forehead and spreads to extremities |
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| 27. What does the Measles rash result from? |
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| 27. infection of the dermal endothelial cells followed by spread to the overlying epidermis |
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| 28. When are Koplik’s spots usually seen? |
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| 28. Before the rash |
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| 29. What is a complication of the measles virus? |
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| 29. Immune suppression – Delayed-type hypersensitivity responses are suppressed, impaired production of antibody and cellular immune responses |
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| 30. What is the primary cause of measles virus-induced immune suppression? |
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| 30. infection of monocytes and other immune effector cells |
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| 31. What 3 things can be neurological MV complications post infection? |
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| 31. 1. Postinfectious encephalomyelitis (PIE), 2. Measles Inclusion Body Encephalitis (MIBE), 3. Subacute Sclerosing Panencephalitis (SSPE) |
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| 32. What is an autoimmune demyelinating disease caused by MV complications? |
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| 32. PIE (postinfectious encephalomyelitis) |
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| 33. What diseases result from the establishment of persistent infections in the brain after MV? |
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| 33. MIBE and SSPE |
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| 34. What is the vaccine for measles? |
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| 34. Live-attenuated measles virus vaccine provides “life-long” immunity |
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| 35. When do Children receive the measles vaccine? |
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| 35. at 12-15 months, 2nd dose at 4-6 years, subcutaneously |
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| 36. Why is the MMR vaccine so effective? |
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| 36. MMR are antigenically stable monotypic viruses |
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| 37. Are there different strains of MV? |
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| 37. Yes, but neutralizing antibody to one strain protects an individual against all circulating strains |
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| 38. How are the different strains of MV defined? |
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| 38. by amino acid differences in the H or HN proteins |
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| 39. Why is measles an ideal candidate for eradication? |
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| 39. 1. only one serotype, 2. clinically identifiable, 3. no animal reservoir, 4. eradication requires “herd immunity” |
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| 40. What is the most common cause of MV resurgence? |
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| 40. Parents choosing not to vaccinate |
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| 41. What are the contraindications for measles vaccination? |
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| 41. Allergic reaction to gelatin or neomycin. Moderately or severely ill at the time of vaccination. Pregnant Women. Anyone on immunosuppressive drugs. |
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| 42. How long should women wait to get pregnant after receiving the Measles vaccine? |
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| 42. 4 weeks |
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| 43. What family is the Mumps virus a member of? |
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| 43. Paramyxoviridae family (rubulavirus genus) |
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| 44. Where does Mumps initially infect? |
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| 44. Nasal mucosa and upper respiratory tract epithelium |
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| 45. Which is more infectious, Measles or Mumps? |
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| 45. Measles |
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| 46. How long is the incubation period for Mumps? |
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| 46. ~18days |
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| 47. What causes the “chipmunk” look of a mumps infection? |
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| 47. Spread to the draining lymph nodes, Infection of the Parotid Gland |
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| 48. What is the first clinical sign of a mumps infection? |
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| 48. Infection of the parotid gland causes “chipmunk” look |
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| 49. When is virus shed? |
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| 49. begins ~6 days before onset of clinical disease |
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| 50. What does half of mumps infection result in? |
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| 50. Virus replication in the CNS |
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| 51. What can virus replication in the CNS lead to? |
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| 51. Aseptic meningitis, Deafness |
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| 52. If you see a truck with some disturbing appendages hanging off the back, what complication did they probably have with the mumps virus? |
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| 52. symptomatic gonadal involvement |
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| 53. What is a major complication of Mumps in post-pubertal men? |
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| 53. symptomatic gonadal involvement – testes swell, can cause sterility |
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| 54. What infection has a correlation with the development of type I Diabetes? |
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| 54. Mumps |
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| 55. What type of vaccine is there for mumps? |
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| 55. Live-attenuated vaccine |
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| 56. Which 2 RNA viruses that cause multi-system infections are (-) stranded? |
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| 56. Measles and Mumps |
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| 57. Which RNA virus that causes multisystem infections is (+) stranded? |
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| 57. Rubella |
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| 58. What is the family of Rubella? |
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| 58. Togaviridae family |
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| 59. What are the 2 genera of Togaviridae? |
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| 59. Alphaviruses and Rubiviruses |
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| 60. How are Rubiviruses distinguished from Alphaviruses? |
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| 60. Rubiviruses have limited host range - Humans |
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| 61. How does Rubella virus replicate? |
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| 61. 1. Enters cell by receptor mediated endocytosis, 2. Genome serves as mRNA 3. Polymerase made first 4. (-) strand antigenome is used as template for both progeny genomes and subgenomic mRNA, which encodes the viral capsid and envelope proteins. |
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| 62. What are the clinical manifestations of the Rubella virus? |
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| 62. Mild disease, Low-grade fever, conjunctivitis and sore throat, lymphadenopathy, Morbilliform Rash |
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| 63. How is does Rubella transmit and replicate? |
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| 63. aerosols, replicates initially in the mucosa of upper respiratory tract and nasopharyngeal lymph nodes |
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| 64. How long is the incubation period of rubella? |
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| 64. ~7-9 days |
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| 65. How long after initial exposure does the morbilliform (maculopapular) rash begin? |
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| 65. 16-21 days |
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| 66. How long can the rubella virus be shed? |
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| 66. Shedding begins after incubation period and continues after rash disappears, can be shed for up to a month after initial exposure. |
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| 67. What is the most devastating effects of Rubella infection? |
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| 67. in fetuses – causes congenital birth defects |
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| 68. When is the highest risk of rubella infections for the fetus? |
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| 68. 1st and 2nd trimester |
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| 69. Infection by Rubella in the first month of pregnancy usually results in what? |
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| 69. spontaneous abortion |
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| 70. What clinical manifestations can be found if a fetus is carried to term by a mother infected by Rubella in the first or second trimester? |
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| 70. Mental retardation, motor disabilities, hearing loss, congenital heart disease, cataracts |
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| 71. What is the primary reason for Rubella vaccination? |
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| 71. directed at protecting the fetus from infection |
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| 72. Why do measles and rubella cause rashes, while Flu, RSV, and hMPV don’t? |
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| 72. Flu, RSV, and hMPV don’t spread beyond Respiratory tract. (class clicker question) |
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| 73. What is most significant about Measles? |
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| 73. it’s Highly Contagious |
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| 74. What was the leading cause of aseptic meningitis prior to development of vaccine? |
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| 74. Mumps |
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| 75. Why is the MMR vaccine so successful? |
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| 75. All three viruses are monotypic, Humans are the only known reservoir |
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| 76. What kind of replication does Parvovirus Have? |
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| 76. Autonomous replication |
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| 77. What is the structure of parvovirus? |
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| 77. Linear, single-stranded DNA, Icosahedra capsid, no envelope |
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| 78. Where does parvovirus replicate? |
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| 78. nucleus |
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| 79. Why does parvovirus need to replicate in rapidly dividing cells? |
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| 79. needs active DNAase |
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| 80. What is “fifth disease”? |
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| 80. Parvo B19 |
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| 81. What are the symptoms of Parvo B19? |
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| 81. erythema infectiosum – a mild common childhood rash |
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| 82. How does Parvo B19 spread? |
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| 82. direct contact with respiratory secretions, prior to rash |
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| 83. What is the Biphasic pathogenesis of parvo B19? |
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| 83. Initial viremia – flu like symptoms; Second Phase – Rash driven by antigenic response |
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| 84. What are the characteristic symptoms of fifth disease? |
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| 84. “Slapped Cheek” rash, Lacy red rash on trunk and limbs |
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| 85. What symptoms can adults have from fifth disease? |
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| 85. Joint pain or swelling, flu like symptoms, Less rash |
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| 86. Who is at risk for transient aplastic crisis caused by Parvo B19? |
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| 86. sickle cell anemia patients |
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| 87. What is the risk for pregnant women who contract parvo B19? |
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| 87. transplacentally transmitted, can result in fetal anemia, hydrops fetalis, miscarriage |
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| 88. What is Parvo B19 sometimes confused with? |
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| 88. Rubella |
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| 89. When are patients most infectious? |
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| 89. prior to rash, difficult to prevent because diagnosis by appearance of rash |
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| 90. What’s the best way to prevent spread of Parvo B19? |
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| 90. Good Hygiene practices |
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| 91. What are the 2 genus of the Poxviridae Family? |
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| 91. Variola virus and Vaccinia virus |
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| 92. What is unique about the Poxviridae structure? |
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| 92. Large non-icosahedral complex structure, Intracellular virus, core and lateral bodies surrounded by envelope; Large double strand linear DNA with proteins |
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| 93. What is unique about Pox replication? |
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| 93. Cytoplasmic Replication, has everything it needs to replicate on it’s own. |
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| 94. In Pox replication, what happens in the uncoating I step? |
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| 94. Virus enters cell, loses outter membrane, releasing core particle into the cytoplasm |
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| 95. What happens in the uncoating II step of Pox replication? |
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| 95. After Early transcription and mRNA translation, Early proteins complete uncoating of DNA and release into cytoplasm, DNA replication begins in cyto |
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| 96. Where are the virus factories for Pox replication? |
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| 96. Cytoplasm |
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| 97. Where does the virus get it’s envelope? |
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| 97. Derived de novo, crescents with no detectable contacts with exiting membranes begin to envelope core structures |
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| 98. What are the pertinent infectious agents in the real world? |
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| 98. Extracellular enveloped virus (EEVs) |
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| 99. What 2 pox viruses specifically cause human disease? |
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| 99. Variola and Molluscum |
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| 100. What does variola cause? |
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| 100. smallpox |
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| 101. What are the 2 basic forms of small pox? |
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| 101. variola major and variola minor |
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| 102. How is Smallpox spread? |
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| 102. inhalation of virus released from ruptured mouth lesions. |
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| 103. Where is the generalized rash of smallpox mostly found? |
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| 103. Head and Limbs |
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| 104. How is Smallpox distinguished from chickenpox? |
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| 104. Small pox – febrile prodrome, firm well defined lesions (like BBs) develop pit (umbilicated), all lesions will be at the same stage. |
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| 105. When is smallpox most contagious? |
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| 105. small red spots in mouth and tongue rupture |
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| 106. How long are patients contagious? |
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| 106. until last scab falls off |
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| 107. What are the 2 forms of Molluscum contagiousum? |
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| 107. Childhood and young adulthood forms |
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| 108. What are the characteristics of Childhood form of molluscum? |
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| 108. –Lesions on face, trunk, and limbs; -spread by direct contact from skin; -mostly tropical |
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| 109. What are the characteristics of the Young adulthood form of molluscum? |
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| 109. Lower abdomen lesions, sexually transmitted |
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| 110. What is vaccinia? |
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| 110. modern day prototype of small pox, lab strain, used for small pox vaccines |
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| 111. What 4 key features are necessary for eradication? |
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| 111. 1. Humans only reservoir, 2. No healthy carriers, 3. No subclinical infections, 4. Effective vaccine afailable |
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| 112. Who should not receive the smallpox vaccine? |
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| 112. Pregnant or breast-feeding women; immunocompromised; People with eczema, atopic dermatitis, or severe acne; non-emergency situations under 18yo, heart disease patients |
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| 113. How can adverse reactions to the smallpox vaccine be treated? |
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| 113. VIG- vaccinia immune globulin |
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| 114. What are some non-life threatening complications of the smallpox vaccine? |
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| 114. generalized vaccinia, inadvertent inoculation, erythema multiforme |
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| 115. What are some Life-threatening complications of the smallpox vaccine? |
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| 115. progressive vaccinia, postvaccinial encephalitis, eczema vaccinatum, myopericarditis or MI |
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| 116. What can a defect in immune globulin cause in a patient receiving the smallpox vaccine? |
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| 116. progressive vaccinia |
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| 117. What family is the Polyoma virus in? |
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| 117. Papovaviridae |
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| 118. What is the structure of Polyoma virus? |
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| 118. circular double-strand DNA genome packaged around histones, non-enveloped icosahedral capsid |
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| 119. How does replication of polyoma occur in permissive cells? |
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| 119. replication and assembly of progeny occurs in nucleus, released by cell lysis |
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| 120. How does replication of polyoma occur in non-permissive cells? |
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| 120. infection leads to transformation of cells, integrates into host chromosome |
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| 121. What can transformation of non-permissive cells lead to? |
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| 121. tumor formation |
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| 122. What are the T antigens responsible for? |
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| 122. Transformation; Small T and large T – immortalize cells, small T and middle T – transform cells |
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| 123. What are the 2 known human polyoma viruses? |
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| 123. BK and JC |
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| 124. Are the human polyoma viruses oncogenic? |
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| 124. No |
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| 125. Where does polyoma initially replicate? |
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| 125. Respiratory of GI tract |
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| 126. What happens after initial infection? |
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| 126. Viremia, passage to kidney, lung, or brain, persistently infect kidney |
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| 127. Who is Polyoma a problem for? |
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| 127. Immunodeficient; transplant patients, AIDS |
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| 128. Where can BK be isolated from? |
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| 128. urine of AIDS patients |
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| 129. What is the etiologic agent of progressive multifocal leukoencephalopathy? |
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| 129. JC |
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| 130. What is PML? |
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| 130. demyelinating disease of CNS, Reactive JC virus infects and lyses oligodendrocytes, Culture not practical, No virus specific treatment |
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| 131. What is the structure of the Herpesvirus? |
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| 131. iscosahedral capsid surrounded by lipid envelope with virus-encoded glycoproteins |
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| 132. Where is Herpesvirus replicated? |
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| 132. Replicated and assembled in the nucleus |
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| 133. What Herpesviruses are neurotropic? |
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| 133. HSV-1, HSV-2, VZV |
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| 134. What herpesviruses are lymphotropic? |
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| 134. CMV, HHV-6, HHV-7, EBV, HHV-8 |
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| 135. What does the primary infection of VZV cause? |
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| 135. chickenpox |
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| 136. What are the symptoms of chickenpox? |
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| 136. fever, itchy rash for 1 week, Late winter/early spring, |
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| 137. What does a reactivated infection of VZV cause? |
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| 137. shingles |
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| 138. Where does the rash occur in shingles? |
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| 138. along the thoracic dermatome |
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| 139. Who is most at risk for CMV? |
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| 139. Transplant Patients! |
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| 140. Where is CMV found in the body? |
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| 140. anything wet – saliva, urine, breast milk, semen, cervical secretions, blood |
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| 141. What cells does CMV infect? |
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| 141. B-cells, causes large, puffed up lymphocyts |
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| 142. What is a diagnostic feature of CMV? |
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| 142. Large Lymphocytes |
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| 143. What does CMV infection in Neonates cause? |
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| 143. deafness and mental retardation |
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| 144. What is the treatment for CMV? |
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| 144. Ganciclovir |
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| 145. What does EBV cause in adolescence? |
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| 145. Infectious mononucleosis |
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| 146. What can EBV cause in AIDS patients? |
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| 146. hairy leukoplakia |
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| 147. What is Burkitt’s lymphoma? |
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| 147. Neoplasm of B-cels that affects bones of the jaw, caused by EBV |
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| 148. What 3 factors is Burkitt’s lymphoma associated with? |
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| 148. Early EBV infection, Activation of c-myc, Malaria |
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| 149. What kind of carcinoma is associated with EBV and a high salt diet? |
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| 149. Nasopharyngeal carcinoma |
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| 150. What types of Herpesvirus cause Roseola? |
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| 150. HHV-6 and HHV-7 |
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| 151. What is the principal symptom of Roseola? |
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| 151. High fever |
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| 152. What herpesvirus is associated with Kaposi’s sarcoma? |
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| 152. HHV-8 |
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| 153. What Herpesviruses are Ubiquitous in all US populations? |
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| 153. VZV EBV HHV-6 HHV-7 |
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| 154. What Herpesviruses are typically acquired in early childhood in the US? |
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| 154. VZV, HHV-6, HHV-7 |
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| 155. What Herpesviruses are sexually transmitted? |
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| 155. HSV-1, HSV-2, CMV, HHV-8 |