Micro Assessment 7 – Flashcards

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