Micro, Ass 6, Renee’s Questions – Flashcards
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| 5. Which proteins on the flu virus are targets for neutralizing antibodies? |
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| 5. Hemagglutinin, Neuraminidase |
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| 6. Which protein is essential for the infectivity of the flu virus? |
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| 6. M2 |
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| 7. What is the replication scheme for the flu virus? |
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| 7. 1. Entry through receptor mediated endocytosis 2. Low pH of endosome required for infectivity 3. Replication in nucleus |
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| 8. Does the flu virus need a symport to release the virus into the host cell? |
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| 8. No, low pH of endosome opens M2 channel and releases virus |
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| 9. Why does the flu virus have to replicate in the nucleus? |
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| 9. mRNA spliced, requires capped mRNAs from host (cap-stealing) |
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| 10. How can Influenza A, B, and C be distinguished ? |
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| 10. Antigenic Differences between their nucleocapsid (NP) and Matrix (M) proteins |
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| 11. What influenza infects Humans only? |
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| 11. Influenza B |
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| 12. What species can the Influenza A virus infect? |
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| 12. humans, pigs, horses, avian species, aquatic mammals |
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| 13. Which flu virus can infect humans and pigs? |
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| 13. Influenza C |
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| 14. How many distinct RNA segments does Flu A and B have? |
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| 14. 8 |
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| 15. Why does Flu C on contain 7 RNA segments? |
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| 15. 2 segments are found on the same protein |
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| 16. Influenza A is subdivided into subtypes and designated by 5 things, whats the only part you need to know about? |
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| 16. The antigenic description of the HA and NA molecules (EX. H3N2, H1N1) |
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| 17. What part of the body is Influenza isolated to? |
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| 17. Respiratory Tract, Upper and Lower |
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| 18. How is Flu mainly spread? |
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| 18. Aerosol droplets (coughing, sneezing) |
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| 19. After infection of Flu virus when do virus titer peak? |
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| 19. 48 hours |
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| 20. How long does it take for a person to stop shedding the Flu virus after infection? |
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| 20. 6-8 days |
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| 21. What does influenza induce in the body that contributes to recovery? |
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| 21. interferon (IFN) |
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| 22. Where is the antibody response found in the body? |
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| 22. Both Serum and Secretory |
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| 23. What is the incubation period for the Flu virus? |
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| 23. Short 24hrs, can be up to 4-5 days |
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| 24. What are the initial symptoms of the Flu? |
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| 24. Headache, chills, and dry cough |
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| 25. What follows the initial symptoms of the Flu? |
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| 25. high fever, myalgias, malaise, anorexia |
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| 26. After the fever resolves from the flu how long can cough and weakness persist? |
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| 26. 1-2 weeks |
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| 27. How do the symptoms of the flu differ in children and adults? |
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| 27. Children have higher fever – can result in convulsions, higer incidence of vomiting and abdominal pain |
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| 28. What are some complications of Influenza if the virus is not cleared? |
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| 28. Primary viral Pneumonia, Combined viral-bacterial pneumonia, Bacterial pneumonia, Reye’s syndrome |
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| 29. What population is at high risk of developing Primary Viral pneumonia after the flu? |
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| 29. Elderly, Patients with cardiopulmonary disease |
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| 30. How soon after onset of illness can influenza progress to Primary viral pneumonia? |
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| 30. 6-24 hrs |
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| 31. If an elderly patient presents with Flu and shortly after develops tachypnea, tachycardia, cyanosis, high fever and hypotension, What are you worried about and how can you treat him? |
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| 31. Primary viral pneumonia, Supportive treatment and Antivirals, monitor for bacterial superinfection |
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| 32. What is a more likely complication of flu then primary viral pneumonia? |
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| 32. Combined viral-bacterial pneumonia |
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| 33. How is viral-bacterial pneumonia distinguished from primary viral pneumonia? |
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| 33. onset is usually delayed in viral-bacterial pneumonia |
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| 34. A patient develops shaking chills, pleuritic chest pain, and productive cough, 4 days after improving from the flu, what’s wrong? |
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| 34. Influenza followed by bacterial pneumonia |
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| 35. What are the most common culprits of bacterial pneumonia after the Flu? |
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| 35. S. pneumonia, S. Aureus, H. influenza |
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| 36. What are some atypical causes of bacterial pneumonia? |
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| 36. M. pneumonia, Chlamydia pneumonia |
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| 37. What syndrome is characteristic of noninflammatory cerebral edema and fatty infiltration of the liver? |
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| 37. Reye’s syndrome |
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| 38. What does Reye’s syndrome result in, how is this tested? |
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| 38. severe hepatic dysfunction, elevated serum transaminase and ammonia levels |
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| 39. What type of Antigenic variation results from minor point mutations in a single HA gene? |
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| 39. Antigenic drift |
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| 40. How does antigenic shift change the Influenza virus? |
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| 40. major antigenic changes that result from replacement of either the HA or NA gene segment (Ex. H1 aH3) |
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| 41. What type of antigenic variation is responsible for most of the major influenza pandemics? |
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| 41. Antigenic Shift |
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| 42. What is the definition of a pandemic strain? |
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| 42. New subtype with no existing human immunity, highly pathogenic, transmitted easily between humans |
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| 43. What type of tests are available to detect influenza A and B? |
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| 43. immunoassay-based nasopharyngeal swabs |
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| 44. How are inactivated vaccines made and how are they administered? |
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| 44. purified virus grown in eggs, whole virus or subvirion, inactivated with formalin or ?-propiolactone, Administered IM |
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| 45. T/F The inactivated vaccine protects against influenza infection. |
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| 45. F – Does not protect against infection but induces resistance to illness |
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| 46. Who is approved for the Live vaccine FluMist? |
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| 46. Healthy kids 2-17, Health Adults 18-49 |
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| 47. This year who does the CDC recommend get the Flu vaccine? |
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| 47. EVERYONE – Universal Influenza Vaccination |
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| 48. Who is the influenza vaccine recommended for? |
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| 48. Pregnant women in 2nd-3rd trimester during flu season, Healthy kids 6mo-5yrs, People 50+yrs, Any age with Chronic medical conditions, Nursing home residents and providers, People who care for those at high risk, Children/Teens with long-term aspirin therapy |
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| 49. How do Amantadine and Rimantadine work as antiviral agents? |
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| 49. Inhibits the M2 ion channel of influenza A |
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| 50. Who are amantadine and Rimantadine used for? |
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| 50. individuals at high risk, people with egg allergies that can’t receive flu vaccine |
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| 51. T/F Resistance to Aniviral Agents can develop. |
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| 51. T – results from single amino acid substitutions in the transmembrane domain of the M2 channel; H3N2 and H1N1 are resistant |
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| 52. How do Neuraminidase inhibitors work as antiviral agents? |
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| 52. inhibit virus release, limiting spread |
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| 53. What are 2 types of Neuraminidase inhibitors? |
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| 53. Relenza (zanamivir), Tamiflu (oseltamivir phosphate) |
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| 54. When do Neuraminidase inhibitors need to be administered to be most effective? |
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| 54. within 48 hrs of symptoms developing |
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| 55. What is different about the Paramyxoviruses compared to the Influenza viruses? |
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| 55. Paramyxoviruses are nonsegmented |
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| 56. What are the characteristics of a paramyovirus? |
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| 56. Consist of 2 Subfamilies, containing 5 genera, Enveloped, Nonsegmented, negative stranded RNAviruses |
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| 57. Where do paramyxoviruses replicate? |
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| 57. Cytoplasm |
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| 58. What is an important characteristic of paramyxoviruses that can cause syncytia formation? |
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| 58. They fuse at the cell surface |
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| 59. What respiratory pathogen is important in infants and children? |
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| 59. Human parainfluenza viruses (hPIV) |
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| 60. What are the major causes of croup? |
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| 60. hPIV 1, 2, and 3 |
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| 61. What are the major causes of pneumonia and bronchiolitis? |
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| 61. hPIV3 |
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| 62. What is hPIV4 linked to? |
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| 62. mild upper respiratory illnesses |
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| 63. Where do PIVs initially infect? |
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| 63. mucous membranes of nose and throat |
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| 64. What can severe hPIV3 infections result in? |
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| 64. bronchopneumonia, bronchiolitis, bronchitis |
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| 65. What are the typical symptoms of hPIV infection in children? |
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| 65. cough, hoarseness and fever |
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| 66. If a childs cough becomes brassy, “seal-like” or barking and stridor ensues, what has developed? |
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| 66. Croup |
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| 67. What other viral infection can cause the same hPIV Croup symptoms? |
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| 67. Influenza A |
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| 68. Chlamydia trachomatis can cause similar symptoms to what virus? |
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| 68. hPIVs |
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| 69. What pathogens can cause bronchitis similar to hPIVs? |
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| 69. Streptococcus pneumonia, Mycoplasma pneumonia |
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| 70. Can symptoms of adenovirus, rhinovirus, or coronavirus be distinguished from mild cases of hPIV infection? |
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| 70. No |
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| 71. When are hPIV 1 and 2 infections most common? |
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| 71. Fall |
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| 72. If croup develops in the winter months what is usually the culprit? |
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| 72. influenza or RSV |
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| 73. How are hPIVs transmitted? |
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| 73. direct contact, large droplet spread |
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| 74. T/F Reinfection with the same serotype of PIV is uncommon. |
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| 74. F – common and can occur relatively quickly |
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| 75. T/F There are no vaccines or antivirals used for hPIVs. |
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| 75. T |
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| 76. What is responsible for many lower respiratory tract infections in children? |
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| 76. Human metapneumovirus (hMPV) |
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| 77. What is the MOST important cause of viral lower respiratory tract disease in infants and children worldwide? |
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| 77. Respiratory Syncytial Virus (RSV) |
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| 78. Where does RSV initially infect? |
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| 78. nasopharynx |
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| 79. If RSV spreads to the lower respiratory tract, how long does it take and what are the symptoms? |
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| 79. 1-3 days, cough and low-grade fever develop |
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| 80. T/F RSV can cause permanent lung damage and the development of asthma. |
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| 80. T |
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| 81. Where can RSV antigens be found? |
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| 81. both epithelium and in exfoliated epithelia cells plugging the airways |
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| 82. T/F RSV is uncommon in adults. |
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| 82. F – common in normal adults; symptoms – rhinorrhea, cough, headache, fatigue, fever |
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| 83. What patients are at high risk for RSV |
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| 83. premature infants, children with chronic lung disease, Premature infants ;1yr at start of RSV season |
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| 84. How is RSV spread? |
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| 84. Large droplet or Fomite contamination |
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| 85. What the heck is a Fomite? |
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| 85. any inanimate object or substance capable of carrying infectious organisms (ex. bedding, cloth, stethoscope) |
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| 86. What is the treatment for RSV infection? |
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| 86. mostly supportive, ensure adequate oxygenation, hydration, and nutrition |
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| 87. What is Synagis (palivizumab) and who is it use for? |
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| 87. recombinant monoclonal antibody that neutralizes RSV, used for high risk infants |
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| 88. What family is Rhinovirus part of? |
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| 88. Picornaviridae |
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| 89. How many serotypes do Rhinoviruses have? |
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| 89. ;100 |
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| 90. What characteristics does the Rhinoviruses have? |
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| 90. Small, non-enveloped, positive-strand RNA virus |
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| 91. What is the distinguishing feature of the mRNA of Rhinovirus? |
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| 91. 5’VPg |
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| 92. What differentiates Rhinoviruses from other picornaviruses? |
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| 92. Inactivated by pH 6.0 or lower |
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| 93. Why is Rhinovirus difficult to grow in culture? |
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| 93. requires reduced temperature (33C) for optimal growth |
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| 94. What does Rhinovirus bind to get into the host cell? |
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| 94. iCAM-1 |
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| 95. How does Rhinovirus exploit the host cell? |
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| 95. IFN and TNF-? upregulate iCAMs, Rhinovirus binds iCAMs |
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| 96. Once the Rhinovirus enters the cell what is the first event that takes place? |
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| 96. Translation of a polyprotein |
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| 97. How are Rhinovirus viral proteins released from the polyprotein? |
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| 97. following specific cleavage events by the virally encoded proteases |
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| 98. How is translation of picornavirus genomes initiated? |
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| 98. cap-independent mechanism |
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| 99. What is the IRES (internal ribosome entry site)? |
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| 99. Sequence near the 5’ end of picornavirus genome that initiates translation |
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| 100. How is translation of picornavirus genomes linked to host cell translation? |
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| 100. Linked to mechanism by which host cell translation is inhibited. |
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| 101. What are the characteristics of a Coronavirus? |
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| 101. Large, Enveloped, positive-stranded RNA virus, Genome capped at 5’ end, has 3’poly A+ tail |
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| 102. What RNA virus has the largest Genome? |
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| 102. Coronavirus |
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| 103. How is the polymerase polyprotein of the coronavirus translated? |
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| 103. 1. cis-cleavage of viral polymerase which synthesizes a (-)sense antigenome, 2. antigenome is template for synthesis of sub-genomic mRNA |
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| 104. What is unique about the coronavirus mRNA synthesis mechanism? |
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| 104. “leader-primed” – results in nested set of overlapping mRNAs with common 3’ end |
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| 105. What allows for a high frequency of recombination in the coronavirus? |
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| 105. “Leader-primed” – polymerase “hopping” |
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| 106. What percentage of Upper respiratory infections does coronavirus cause in humans? |
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| 106. 15-20% |
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| 107. What “severe atypical pneumonia” was caused by a coronavirus in 2003? |
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| 107. SARS |
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| 108. T/F coronaviruses cause a significant amount of GI problems? |
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| 108. T |
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| 109. What do Rhinovirus and coronavirus infections do to the nasal mucosa? |
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| 109. Cause shedding of the ciliated epithelium |
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| 110. Why are conventional vaccinations not feasible for coronaviruses and rhinoviruses? |
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| 110. Large # of serotypes for rhinoviruses, high frequency of recombination for coronaviruses |
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| 111. What is Structure of Adenovirus? |
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| 111. Linear, double-stranded DNA genome, 36 kilobase pairs, No envelope |
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| 112. What does Adenovirus cause infection in? |
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| 112. Respiratory, Eye, GI |
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| 113. What is Adenovirus stable against? |
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| 113. detergents, low pH |
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| 114. How many serotypes of Adenoviruse are known to infect humans? |
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| 114. 49 |
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| 115. Where does replication and assembly of Adenovirus occur? |
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| 115. Nucleus |
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| 116. How is adenovirus spread? |
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| 116. Respiratory or fecal-oral route |
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| 117. What Bug is associated with pharyngoconjunctival fever in children? |
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| 117. Adenovirus |
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| 118. Conjunctivitis that feels like “sand in the eye” is caused by what bug? |
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| 118. Adenovirus |
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| 119. What is the main pathogenic species of Pseudomonads? |
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| 119. P. aeruginosa |
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| 120. What bug is widely distributed in nature and is highly resistant to antibiotics and can rapidly evolveresistance? |
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| 120. Pseudomonads |
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| 121. What characteristics do Pseudomonas have? |
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| 121. Gram Negative, motile, aerobic rods, Produce Soluble Pigments |
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| 122. What allows pseudomonas to grow just about anywhere? |
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| 122. Obligate aerobes – can us CO2, atmospheric ammonia, nitrogen sources |
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| 123. An organism that grows at 42C is diagnostic for what bug? |
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| 123. Pseudomonas |
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| 124. What do cultures of Pseudomonas smell like? |
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| 124. Grapes |
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| 125. What type of pigmented siderophores do pseudomonas produce and what color are they? |
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| 125. Pyocyanin – Blue, Pyoverdin – fluorescent yellow pigment |
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| 126. What do some strains of pseudomonads produce that is induced in the CF lung? |
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| 126. Alginate |
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| 127. What does an overproduction of alginate result in? |
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| 127. mucoid phenotype |
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| 128. Who do pseudomonads cause a problem for? |
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| 128. immune suppressed people |
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| 129. What type of toxin do pseudomonads produce? |
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| 129. Exotoxin A |
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| 130. How does Exotoxin A effect the cell? |
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| 130. causes necrosis by blocking protein synthesis |
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| 131. What 2 toxins have an identical mechanism of blocking protein synthesis, but are produced by different bugs? |
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| 131. Exotoxin A and diphtheria |
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| 132. What bug is associated with Swimmers ear frequently? |
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| 132. Pseudomonas |
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| 133. What type of rash can you get if you are on a medical conference and you shave your legs before going into a hot tub that doesn’t have enough chemicals? what bug caused it? |
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| 133. Hot Tub Folliculitis, Pseudomonas |
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| 134. How are pseudomonas infections treated? |
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| 134. Combined therapy to limit resistance |
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| 135. What are the characteristics of Acinetobacter? |
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| 135. Ubiquitous aerobic gram negative coccobacillus |
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| 136. How does Acinetobacter infect? |
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| 136. compromised patients – low pathogenic potential |
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| 137. What strain of Acinetobacter is most common? |
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| 137. A. baumanii |
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| 138. What bug has recently been a major problem in the Burn Wards of Memphis? |
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| 138. A. baumanii |
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| 139. What pathogen is A. baumanii easily mistaken for? |
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| 139. N. meningiditis |
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| 140. How is A. baumanii differentiated from Neisseria? |
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| 140. oxidase negative |
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| 141. Why is antimicrobial testing necessary to guide therapy of Actinobyces? |
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| 141. Extremely resistant to antibiotics |
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| 142. What bug shows biopolar metachromic granules? |
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| 142. B. pertussis |
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| 143. What bug is a small gram negative coccobacillus that looks like H. influenza? |
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| 143. B. pertussis |
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| 144. Why do you have to let the lab know before you culture someone you suspect as having whooping cough? |
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| 144. requires an enriched and selective medium for primary isolation – Bordet-Gengou medium |
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| 145. How is B. pertussis transmitted? |
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| 145. droplet inoculation |
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| 146. What does B. pertussis produce a lot of that causes irritation, inflammation, and cough? |
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| 146. AB exotoxins |
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| 147. Does B. pertussis invade the ciliated epithelium? |
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| 147. No, multiples on epithelia without invasion |
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| 148. What controls the virulence gene expression of B. pertussis? |
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| 148. bvgA/bvgS two component regulatory system |
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| 149. What is the enzymatic action that is specific for the Pertussis toxin? |
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| 149. Interfere with PMN, monocyt, and macrophage function, Lymphocytosis, Sensitization to histamine, Hypoglycemia |
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| 150. How does the BvgS/A system regulate virulence factors? |
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| 150. BvgS senses a stimulus, phosphate from a donor transferred to BvgS eventually goes to BvgA which Activates transcription of several genes. |
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| 151. How Does Pertussis A toxin interfere with normal function? |
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| 151. Conversion of ATP to cAMP cannot be stopped because the Gi protein that normally inhibits adenylate cyclase is inhibited by A toxin. |
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| 152. How long is the incubation period for B. Pertussis? |
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| 152. 1-2 weeks |
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| 153. When are patients most infections with B. Pertussis? |
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| 153. Catarrhal stage |
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| 154. How is the paroxysmal stage of B. pertussis characterized? |
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| 154. coughing fits – with whoop inhalation, lasts about 2 weeks, high white blood cell count |
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| 155. How is B. pertussis diagnosed? |
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| 155. primary by clinical features, Nasopharyngeal swap |
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| 156. Whats the drug of choice for B. pertussis? |
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| 156. Erythromycin |
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| 157. How is B. pertussis prevented? |
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| 157. DTap immunization |
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| 158. What bug is a Gram positive Rod that appear in clumps resembling Chinese letters? |
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| 158. C. diphtheriae |
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| 159. Where is C. diphtheriae found? |
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| 159. Human reservoir – not found anywhere else in nature |
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| 160. T/F Production of diphtheria toxin only occurs in cells that have been transduced with a phage that carries the toxin genes. |
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| 160. T |
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| 161. What is the expression of the Diphtheria toxin dependent on? |
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| 161. iron – Low concentrations increase toxin production, High concentrations repress production |
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| 162. What type of toxin is the Diphtheria toxin? |
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| 162. AB toxin (like pseudomonas) |
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| 163. What tissues are most affected by Diphtheria toxin? |
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| 163. myocardium and peripheral nerves |
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| 164. What does the A subunit of Diphtheria toxin inhibit? |
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| 164. polypeptide elongation in the presence of NAd by inactivation of EF-2 |
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| 165. What is the characteristic pathology of Diptheria toxin? |
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| 165. pseudomembrane over tonsils, pharynx, and larynx |
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| 166. What bug can cause the characteristic “bull neck”? |
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| 166. C. Diptheria |
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| 167. What is the mainstay of therapy for Diphtheria? |
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| 167. Antitoxin – immediately |
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| 168. What is the characteristic stain of Mycobacteria? |
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| 168. Acid fast stain positive |
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| 169. What is unique about the M. Tuberculosis envelope? |
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| 169. Mycolic Acid, Cord Factor, Wax-D |
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| 170. What properties are associated with the high concentrations of lipids in the cell wall of M. tuberculosis? |
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| 170. Impermeability to stains and dyes, Resistance to antibiotics, acidic and alkaline compounds, osmotic lysis, lethal oxidations, desiccation |
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| 171. When do Tubercles form with tuberculosis infection? |
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| 171. Primary Disease |
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| 172. What are calcified tubercles seen called? |
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| 172. Ghon complexes |
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| 173. In the absence of CMI, how can TB progress? |
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| 173. Miliary TB |
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| 174. What test for TB indicates infection but does not indicate disease? |
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| 174. PPD |
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| 175. How long do cultures of TB need to be kept to rule out disease? |
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| 175. 1-2 months |
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| 176. What is the treatment plan for TB? |
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| 176. Combined therapy - Isoniazid, Rigampin, pyrazinamide, and ethambutol or streptomycin, 6-9 months, patients are non-infectious within 2 weeks but not cured |
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| 177. What is Cord Factor for? |
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| 177. virulence factor that functions to inhibit PMN migration |
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| 178. What are the characteristics of Actinomyces? |
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| 178. Club-shaped, gram + rods that form Branched filaments. |
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| 179. What do the microcolonies of actinomyces in pus look like? |
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| 179. sulfur granules |
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| 180. What is the reservoir of Actinomyces? |
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| 180. Human oral and GI |
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| 181. What is Actinomyces israelii nearly always associated with? |
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| 181. Trauma and compromised immunity (surgery, tooth extraction, IUDs) |
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| 182. What Disease is characterized by “lumpy jaw”? |
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| 182. Cervicofacial actinomycosis |
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| 183. What is the treatment for Actinomyces? |
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| 183. Prolonged Penicillin |
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| 184. Where is Nocardia found? |
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| 184. Soil |
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| 185. What does Nocardia resemble? |
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| 185. Aerobic weakly gram positive branching rods that look like fungi |
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| 186. What kind of acid stain do Nocardia have? |
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| 186. weakly acid fast |
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| 187. T/F Nocardiosis are Penicillian resistant. |
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| 187. T – use Trimethylprim-sulfamethoxazole |
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| 188. Does Atypical Pneumonia always include fever? |
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| 188. No – may or may not, radiological evidence may distinguish |
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| 189. How does growth of Chylamydia occur? |
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| 189. biphasic developmental cycle |
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| 190. What is a significant cause of community acquired pneumonia? |
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| 190. Chlamydia pneumonia |
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| 191. What are the characteristics of Chlamydia? |
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| 191. Gram-negative spherical bacteria that are obligate intracellular parasites |
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| 192. What is the developmental cycle of Chlamydiae? |
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| 192. Elementary Bodies attach and enter cell, Primary Differentiation, Cell division, Rapid multiplication, Effector secretions, Secondary differentiation, EB released and Reinfect |
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| 193. What bug is associated with chronic atherosclerotic disease? |
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| 193. Chlamydia Pneumoniae |
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| 194. What are the 3 predominant bacterial causes of Atypical Pneumonia? |
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| 194. Chlamydia, Mycoplasma, Legionella |
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| 195. What is the smallest free-living organism? |
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| 195. Mycoplasma |
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| 196. T/F Mycoplasma lack a cell wall. |
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| 196. T |
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| 197. What are the symptoms of Mycoplasma pneumoniae, and who do they typically occur in? |
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| 197. Mild respiratory infection, sore throat and pharyngitis, occur in 1-5 YO |
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| 198. How does mycoplasma activate inflammatory cytokines? |
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| 198. lipoproteins interact with alveolar macrophage Toll-like receptors |
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| 199. T/F Mycoplasma will not show up in a blood test. |
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| 199. F – Positive blood test after 10 days of infection |
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| 200. What is used to Treat M. pneumonia? |
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| 200. 2nd Generation – Macrolides, Tetracyclines, Fluoroquinolones |
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| 201. What are the characteristics of Legionella? |
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| 201. Aerobic Gram Negative Rod, facultative intracellular bacteria |
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| 202. What is Legionnaires Disease? |
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| 202. more severe pneumonia form of L. pneumophila infection |
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| 203. What temperatures are Legionella dormant, have ideal growth, and survive but don’t multiple? |
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| 203. Dormant ;20C, Ideal Growth Rate 20-50C, Survive but don’t multiple ;50C |
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| 204. Where does L. pneumophila replicate? |
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| 204. alveolar macrophages after inhalation |
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| 205. How does L. pneumophila avoid phagosome-lysosome fusion? |
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| 205. creating a specialized vacuole that resembles the endoplasmic reticulum of the host |
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| 206. Who does L. pneumophila most often infect? |
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| 206. middle age to older patients, smokers, chronic lung disease patients and immunocompromised |
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| 207. How is L. pneumophila treated? |
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| 207. Macrolides, fluoroquinolones |
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