Immunology Final Lectures 1-5

  1. what type of bacteria is chlamydia
    obligate intracellular parasite
  2. What are the two morphologically distinct forms of chladmydia
    • larger, noninfectious reticulate body
    • smaller, infectious elementary body
  3. what is the most common bacterial sexually transmitted infection in humans and are the leading cause of infectious blindness in the world?
    C. trachomatis
  4. WHO initiative to prevent trachoma (SAFE)
    • Surgery
    • Antibiotics
    • Facial-cleanliness
    • Environmental improvement
  5. C. psittaci is what kind of disease?
    Ornithosis (spread by birds)
  6. what is a worldwide cause of community acquired respiratory infection?
    C. pneumoniae
  7. Chlamydia are sensitive to what kind of antibiotics?
    Certain broad-spectrum 

    NOT PCN!!!
  8. T/F: mycobacteria are spore-forming and motile
    • FALSE
    • they are NON-spore forming and are NOT motile
  9. What is unique about mycobacteria's cell surface?
    It contains mycolic acid and this makes it hydrophobic which allows it to evade chemical disinfectants (strong acids and bases)
  10. Mycobacteria are resistance to _____ but not to _____ or _____
    • dessication
    • UV radiation
    • heat
  11. what can mycobacteria (such as M. tuberculosis) be stained with?
    Ziehl-Neelsen stain
  12. Mycobacteria are acid-fast which means what?
    Once stained they are not decolorized by acidified solvents

  13. Mycobacterium causes ____ which is known as ____ disease
    • Leprosy
    • Hansen's
  14. Leprosy is a continuum between two poles: what are these two poles?
    Tuberculoid Leprosy which progresses to lepromatous leprosy
  15. What other mammals gets leprosy besides humans?
  16. What caused the incidence of TB to rise in the early 1990s and in other parts of the world?
    it rose in association with HIV--immune system was compromised so you couldn't keep TB at bay
  17. T/F: M. tuberculosis is aerobic affects the lungs so this makes sense
  18. How can TB spread (2)
    • respiratory droplets (through exhalation)
    • through unpasteurized milk (bovine TB)
  19. M. tuberculosis induces a _____ and a _____ response
    • Cellular (with T cells) 
    • Humoral (with antibodies)
  20. T/F: antibodies confer resistance to the pathogen

    it is the CD4+ cells and the accompanying delayed-type hypersensitivity directed against bacterial antigens that contribute to immunity and pathology of TB
  21. why does M. tuberculosis cause a stronger T cell response?
    because it is intracellular and so the T cells attack it because they attack things inside the cells
  22. What percentage of primary TB cases lead to arrested infection?
  23. What percentage of primary TB cases that have arrested lead to secondary TB (reactivation)?
  24. How does M. Tuberculosis replicate inside of macrophages?
    because they prevent the fusion of the phagosome with the lysosome
  25. T/F: tubercles are only found in the lungs
    False! they can be found in other parts of the body too
  26. what is miliary TB?
    TB that is extra pulmonary (spread to other parts of the body)
  27. T/F: The larger induration with the Mantoux test, the more aggressive the TB is
    • FALSE--doesnt give quantitative information
    • just a yes or not whether you have TB or not
  28. What are the two ways that M. tuberculosis can be identified and what is more accurate
    • 1. cultured then visualized Ziehl-Nelson stain 
    • 2. amplification via PCR

    PCR is more accurate because there are risks of artifacts with the stain technique
  29. Why is it necessary that the usual TB treatment begin with combination antibiotic therapy?
    Because some M. tuberculosis exhibit resistance to one or more of the primary drugs (antibiotics or chemotherapeutic agents)

    MDR-TB--> multi-drug resistant TB
  30. Four ways combination antibiotic therapy works
    • 1. Broadens the antibacterial spectrum--> microbe is assaulted by more than one so if one AB doesn't kill it another could 
    • 2. There might be secondary infections with the TB so the antibiotics help kill these
    • 3. Synergy with multiple antibiotics
    • 4. Destroys the possibility of resistance--> TB might be resistant to A but not B
  31. What are the two antibiotics used with TB and how do they work?
    • Rifampin/Rifampicin--> stops transcription
    • Isoniazid--> works to prevent the synthesis of mycolic acid (fatty acid synthases)
  32. What is a problem with isoniazid?
    It blocks the niacin in your body and can cause problems with pellagra
  33. what is the treatment with someone who is TB positive but asymptomatic (latent TB)
  34. Bacille Calmette Guerin is a attenuated vaccine against what?
    TB (but contains M. bovis strain)

    NOT recommended or used in the US --> only for very high risk people 

    Not very effective and can interfere with mantoux test
  35. T/F: you can tell if a latent disease is infectious
    FALSE--no way of telling

    latent TB is NOT INFECTIOUS

    but latent herpes simplex is infectious
  36. What are the three things that Ricksettia, Erlichia, Anaplasma,and Coxiella share
    • obligate intracellular parasites
    • most infectious caused by them are transmitted by arthropods
    • diseases caused by them are systemic diseases
  37. thought to be the closest living relative to the ancestral free-living organism that became mitochondria
    R. prowazeki
  38. Rickettsia causes what disease? and what transmits it?
    Rocky Mountain spotted fever

    transmitted by infected ticks 

    other spotted fevers--> rickettsialpox
  39. T/F: the lice infected by R. prowazeki are eventually killed by the bacteria
  40. endemic typhus (NOT TYPHOID--causes by salmonella) is caused by what and is transmitted by what?
    • caused by R. prowazeki
    • transmitted by infected lice
  41. papovaviruses, adenoviruses, and parvoviruses are what kind of viruses?
    non-enveloped, DNA viruses
  42. what lesions do the 150 types of HPV induce in their hosts?
    hyper plastic epithelial lesions
  43. transmission of HPV requires ____ __ with an infected individual or a fomite or to a _____ during the ___ process
    • Direct contact
    • Neonate
    • Birth
  44. What develops as a results of cell multiplication and delayed differentiation induced by the HPV
    A wart
  45. Virally encoded proteins by HPV can bind to and inhibit what?
    p53 and pRb proteins

    these are tumor suppressor genes
  46. What correlates with a high risk for developing cancers with HPV?
    the affinity binding between the viral protein and tumor suppressor proteins
  47. with HPV warts the progression of malignancy occurs primarily in warts located where?
    on mucosal surfaces
  48. How does HPV causing cancer help the virus?
    • it allows it to spread
    • More cells replicating with the virus in the cell --> more virus
  49. What is the difference between a provirus and an episome
    a provirus is when the viral genome is integrated int eh host genome 

    an episome is when the virus replicates as an individual body inside the cell (this is what HPV does)
  50. HPV strains that cause genital papillomas
    HPV 6 and 11
  51. HPV strains that cause cervical cancer and other cancers such as anal, penile, vaginal, vulvar and oropharyngeal
    16 and 18

    the are the more high risk types
  52. Cutaneous warts are caused by what HPV types?
    oral and nasopharyngeal mucosal surface infections?
    HPV 1-4

    HPV 13 and 32
  53. What are two types of screening tests for cervical cancer and which is more effective and accurate
    Pap smear (cytology --> looking for the presence of abnormal cells)

    PCR (looking for presence of more aggressive viruses)

    PCR recently found to be more accurate and efficient
  54. What is the problem with excising warts or destroying the wart tissue?
    The HPV is still present in the surrounding tissue and can cause recurrence of warts
  55. What is the rug treatment for HPV warts? (2)
    • Topical DNA synthesis inhibitor
    • Oral administration of interferon
  56. Guardasil, a vaccine for HPV contains capsides for what four HPV types? why these?
    6,11,16 and 18

    these are the most aggressive
  57. polyoma viruses can do what?
    causes tumors in culture and in species other than humans (not know to cause tumors in humans)

    Polyoma--> means many tumors
  58. What are the three polymer viruses?
    • BKV
    • JCV
    • MCV
  59. What virus (specifically types 4 and 7) has a live, attenuated vaccine specifically for military personnel?
  60. the single human pathogen among the parvoviruses is
  61. B19 can cause the following (3)
    • Transient aplastic crisis in patients with sickle cell
    • erythema infectiosum (fifth disease)
    • birth defects (spontaneous abortion rate elevated in first trimester of the disease)
  62. The herpes virus genome is relative ____ for a virus
  63. Clinically, why is it good that the herpes virus is relatively large?

    **THIS will be on the exam!!
    If it is larger, each protein that is produced can serve as a potential target for a therapeutic drug
  64. T/F: non-enveloped viruses are more pathogenic than enveloped
    FALSE--> you CANNOT make any statements on which virus is more pathogenic just based on its envelope or lack thereof
  65. T/F: if you don't have herpes blisters than the virus is not contagious

    Even if you don't have blisters the virus can still be contagious because of viral shedding (virus leaving the host)
  66. What are the three subfamilies of herpes viruses
    • The herpes simplex group (HSV 1, HSV2 and varicella zoster virus)
    • The cytomegalovirus group (HCMV and HHV 6 and 7)
    • The lymphoproliferative group (EBV and HHV 8)
  67. why are VZV and HSV in the same sub family?
    They have many genes that have sequence identity
  68. Where do the HSV 1 and 2 establish latency?
    nerve ganglia
  69. What type of cells do CMV produce?
    Large cells with multiple nuclei (because fused)

    CMV is enveloped and it makes sense that it fuses the membranes together because it works on the level of the membrane
  70. Where does EBV and HHV 8 establish latency?
    primarily in B cells
  71. Because EBV and HHV8 establish latent infections in B cell what do they do to these cells?
    they can induce proliferation and immortalization of lymphoblastic cells (early lymphocytes)
  72. Why is the transcription of herpes virus called cascade control?
    Because it is a cascade of transcription and this sequence is very regulated and structured
  73. T/F: HSV 1 and HSV 2 have very low sequence identity
    FALSE--> they have about 50% sequence identity which is very high (very similar)
  74. How are HSV 1 and 2 transmitted
    By direct contact with the virus containing bodily secretion (prevents drying out of the virus) or by contact with lesions on mucosal or cutaneous surfaces
  75. T/F: HSV 1 is only found above the waist and HSV 2 below the waist

    often times is true but can have either virus in either place
  76. What are the most common symptoms of herpes infection in the upper body (3)
    • gingivostomatitis in children
    • pharyngitis or tonsillitis in adults
    • kertaoconjunctivitis (can cause corneal scarring and eventually blindness)
  77. In pregnant woman with primary HSV infection, the risk of infecting the newborns during the birth process is ____ (percentage)
    30-40% (very high)
  78. T/F: transplacental infection of HSV is very common
    False--> it rarely occurs
  79. reactivation of latent HSV can be caused by what 4 factors
    • hormonal factors
    • fever
    • psychological stress
    • physical damage of the neurons
  80. Reactivation of HSV_  genital infections can occur with greater frequency can HSV _
    • 1
  81. The presence of HSV in human cell tissue culture can result in the formation of ____
    syncytia (fusion between cells)
  82. What is the name of the drug (guanine analog) used to treat HSV and primary varicella
  83. How does Acyclovir work
    It is a guanine analog and it resembles guanosine and therefore gets phosphorylated by HSV thymidine kinase and it gets incorporated in the growing chain of viral DNA and it is not compatible with chain elongation so it leads to chain termination and eventual killing of the virus
  84. Is there a vaccine for HSV
  85. Primary infection of VZV causes ______ while reactivation of the latent viruses causes _____
    • chicken pox
    • shingles
  86. Varicella is more severe among ___ than among ___
    • adults 
    • children

    Childhood diseases are more severe in adults
  87. An acute encephalopathy that can sometimes follow VZV or influenza infection and is associated with administration of aspirin to children to treat pain during the viral illness or during recovery
    Reyes syndrome
  88. What type of vaccine is the chicken pox vaccine
    live, attenuated
  89. What can be given to someone who has never been immunized or who you think has come into contact with someone who chicken pox or shingles?
    Varicella-zoter immunoglobulin
  90. What is the vaccine for shingles called
  91. T/F: shingles can be passed on from person to person
    False-->chicken pox is what is passed on but the reactivated viruses can cause shingles
  92. The small pox genome is relatively ____ DNA genome
    large (codes for more than 200 proteins)
  93. What is unique about the replication cycle of the smallpox DNA virus?
    it occurs in the cytoplasm

    Since it is DNA you would assume it occurs in the nucleus
  94. Smallpox has been eradicated through vaccination with
    live vaccina virus (a close relative to the virus that causes cowpox)
Card Set
Immunology Final Lectures 1-5
Exam 3 Material