Slow CNS Infections Microbiology

  1. Poliovirus is of ____ family. What other virus is within the same family?
    • Picornaviridae – an enterovirus
    • Coxsackie A and B
    • Echovirus
  2. Poliovirus genome:
    • ssRNA +
    • non-segmented
    • no envelope
    • replicate in cytoplasm
  3. T/F: humans are the only reservoir for poliovirus
  4. How many antigenic serotypes for poliovirus?
    3 antigenic serotype – outer capsid proteins
  5. T/F: antibodies against 1 antigenic serotype of poliovirus has cross-protection for the other 2 antigenic serotypes
    False; there is no cross-protection, need to make antibodies against each type
  6. T/F: Poliovirus is transmitted fecal-orally and it is a very efficient at infecting, if swallowed from say contaminated water or surfaces, will get infected
    True
  7. Polio virions accumulate in the cell’s _____, and are released upon ____.
    • Cytoplasm
    • Lysis and death of the cell
    • (does NOT bud off from the cell membrane, it causes cell death)
  8. T/F: most poliovirus infection are asymptomatic
    True
  9. Abortive poliomyelitis presents with _______, without _______
    • Flu like symptoms
    • Without CNS symptoms – hence “abortive”
  10. T/F: Aseptic meningitis is paralytic
    False; it is non-paralytic. Paralytic poliomyelitis is paralytic
  11. What is Paralytic poliomyelitis?
    • Flaccid paralysis of limb muscles. Though rare, <2% of infections result in this
    • Paralysis of respiratory muscles 2/2 bulbar poliomyelitis affecting medulla oblongota
  12. What is post-polio syndrome?
    Progressive muscle weakness, fatigue and atrophy about 30-40 years after poliomyelitis episode as a child due to reinnervated motor neuron dying off causing muscle to atrophy
  13. Poliomyelitis risk factors goes up with _____, and ______ women
    • Age
    • Pregnant
  14. T/F: Poliovirus enters the body and attack muscle cells by killing myocytes causing paralysis
    False; virus attack and kill motor neurons, not direct attack to muscles.
  15. Where in the spinal cord does poliovirus infect?
    Anterior horn, replicates in the motor neurons
  16. T/F: no permanent carrier state occurs following infection by poliovirus, but virus excretion in the feces can occur for several months
    True
  17. How is polio diagnosed?
    • Viral isolation using stool, throat swab or CSF
    • Antibody titer (though won’t show antibody in minor illness)
  18. T/F: polio can be treated with acyclovir
    False; acyclovir targets DNA virus, polio is ssRNA+. Only treatment is supportive care, there is vaccine that can prevent
  19. Injected polio vaccines are _____, will not revert to become pathogenic; while Oral vaccines are ____ and may revert to virulence and cause disease in immunocompromised
    • Inactivated- injected (salk)
    • Live, attenuated – oral (sabin)
  20. Live (Sabin)/Oral polio vaccine _____ IgA, _____ IgG, and _____ transmission
    • Produces
    • Produces
    • Interrupts
  21. Killed (salk)/Injected polio vaccines ____ IgA, ___ IgG and ____ transmission
    • Does not induce
    • Induces
    • Does not interrupt
  22. Rabies encephalitis is part of _____ family
    Rhabdoviridae
  23. Rhabdoviridae genome:
    • Enveloped
    • ssRNA negative
    • linear
    • non-segmented
    • replicates in cytoplasm
  24. What allows rhabdoviridae virus to have cell contact?
    Glycoproteins on their envelope
  25. T/F: like poliovirus, rabies kill the infected host cell
    • False; unlike poliovirus, rabies do not kill the infected cell, instead it buds off
    • Typical negative sense ssRNA shit
  26. Incubation period of rabies in human:
    • 1-3 months
    • Depending on host age, immune status, viral strain, etc
  27. T/F: bit by a face with a rabied dog is worse than getting bit on the foot
    Yes, because the face is closer to the brain
  28. Presentation of rabies in human (progressive encephalitis):
    • Agitation, paralysis, anxiety, hallucination
    • Hydrophobia (hates water)
    • Hypersalivation
    • Aerophobia (fear of flying)
  29. Wil reservoirs of rabies:
    • Raccoons
    • Skunks
    • Bats (most cases of human rabies in the US have had bat exposure)
    • Foxes
    • Coyotes
  30. Domestic mammals reservoir for rabies?
    • Cats, dogs, cattle
    • (sylvatic-urban rabies)
  31. T/F: contact with saliva, brain/ nervous system tissue of an infected animal is how Rabies is transmitted
    True; usually though a bite wound
  32. Where does the rabies virus replicate in our body?
    Muscles or connective tissue at the site of inoculation (bite site)
  33. Diagnosis of rabies in human:
    • Saliva test for virus isolation or RT-PCR (if found in saliva though = bad news)
    • Serum and spinal fluids for antibodies
    • Skin biopsy for rabies antigen
  34. Negri bodies, think:
    Rabies!
  35. What are negri bodies?
    Specific eosinophilic cytoplasmic inclusion found in rabies-infected nerve cells
  36. Post-exposure therapy for Rabies:
    • Rabies immune globulin (HRIG) near the wound – passive immunization
    • Inactivated rabies vaccines in four doses (away from the wound)- active immunization to develop long term protection
  37. JC virus causes ____
    • Progressive multifocal leukoencephalopathy (PML)
    • can have hydrocephalus
  38. JC virus is of the ___ Family. With genome:
    • Polyomaviridae
    • Double-stranded Circular DNA
    • Non-enveloped
  39. T/F: Like poliovirus, JC virus is also cytolytic, meaning that it kills the infected cell
    True
  40. T/F: 80% of people have been exposed to JC virus in childhood (likely through inhalation of the virus) but this is asymptomatic, and the virus remains quiescent in kidneys, bone marrow, lymphoid tissues
    True
  41. How is JC virus activated from its quiescent state?
    Severe immunosuppression such as HIV or organ transplant
  42. What happens with the brain in progressive multifocal leukoencephalopathy caused by JC virus?
    • Demyelinating disease of the White matter, killing oligodendrocytes
    • Fatal
  43. What Is Creutzfeldt-Jakob Disease?
    Caused by prions.
  44. Prion is a _____ and it ____ nucleic acid
    • Protein- proteinaceous infectious particle
    • Does not have
  45. How does a regular protein become a prion?
    Misfolded beta sheets proteins aggregate; “self-propagate” converting normal proteins into these bad ones
  46. T/F: prions are not living, not a virus and resistant to proteases
    True
  47. Normal cellular protein is PrP__and spontaneous mutation occurred, causing post-translational conformational change changing it to PrP___
    • PrPC
    • To become PrPSc – aka Scrapie
  48. PrPSc (arises from either spontaneous mutation or inculated) starts converting normal endogenous PrPc protein from mostly _____ to having _____
    • Alpha-helices (normal PrPc)
    • Beta sheets (mutated PrPsc)
  49. What eventually happens when there is accumulation of PrPSc ?
    • Causes cell death, death of brain tissue
    • Spongiform encephalopathy- huge gaps in neuronal tissue
  50. T/F: formation of PrPsc prion proteins yield minimal immune response, not enough to combat the rate at which these proteins are aggregating
    False; there is no immune response at all because these are still considered “self” proteins so body can’t do anything about it
  51. 3 ways to get prion:
    • Sporadic (for unknown reason, random ass mutation)
    • Inherited (super rare)
    • Acquired (from medical procedure or contaminated food like mad cow)
  52. Diagnosis of human prion disease:
    • Western blot
    • Protein in CSF
    • Protein misfolding cyclic assay
Author
lykthrnn
ID
348770
Card Set
Slow CNS Infections Microbiology
Description
HemeOnc Final
Updated