Micro, Ass 6, Renee’s Questions – Flashcards

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1.       What are the characteristics of the Influenza virus?
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1. Enveloped, with segmented, single-stranded, negative-sense RNA genomes
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2. What part of the influenza virus must fuse with the host cell membrane to transfer the virus?
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2.       Envelope
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3. What is the basis for emergence of new pandemic strains?
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3.       segmented genome allows reassortment
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4. What 3 proteins are located on the influenza envelope?
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4.       Hemagglutinin, Neuraminidase, M2
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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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