NMSK B Exam 2 Microbio

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NMSK B Exam 2 Microbio
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2013-11-10 20:41:50
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Microbio for week 3/4
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  1. 1. How would you describe a brain abscess?
    2. What are the neuro symptoms?
    3. Most commonly cultured organism from a brain abscess?
    • 1. A focal intracerebral infection that is characterized by pus filled with dead/live microorganisms.
    • 2. Low-grade fever, dull/achy headache 
    • 3. Streptococci
  2. What would you see in a CSF analysis of a patient with chronic meningitis? (TB, fungal)
    • 1. Normal/slight increased pressure
    • 2. Spider-web clotting
    • 3. Increased protein ~225
    • 4. PMNs predominates then lymphocytes.
    • 5. Acid-fast for TB, India ink for fungal cases
  3. How does transmission occur for Cryptococcus species? (C. neoformans, C. gattii)
    • 1. Inhalation of spores
    • 2. Desiccation of yeast cells
  4. 1. What is the environmental source of C. neoformans?

    2. What is the immune status of those affected?
    1. Bird droppings

    2. Immunocompromised
  5. 1. What is the environmental source of C.gattii?

    2. What is the immune status of those affected?
    1. Eucalyptus trees

    2. Immunocompetent
  6. Name the 2 important virulence factors of Cryptococcus species
    1. polysaccharide capsule to prevent phagocytosis and survive within macrophage.

    2. Melanin to protect against oxidative killing
  7. What are the clinical manifestations of Cryptococcus species?
    • Cryptococcus species = chronic meningitis:
    • -Headache
    • -Nuchal rigidity
    • -Seizures
    • -Disorientation
    • -Pneumonia
    • -Cryptococcomas (granulomas) mostly in C. gattii
  8. How do you diagnose Cryptococcus species?
    • 1. Stain: India ink
    • 2. CSF analysis: white mucoid colonies
    • 3. CrAg: capsule antigen testing
    • 4. MRI/CT: for cryptococcal lesions
  9. Where can C. neoformans be found?
    The soil, due to bird droppings.
  10. What are some predominant symptoms of C. neoformans?
    • 1. Bird-droppings --> inhalation --> pneumonia, shortness of breath, cough, fever.  
    • 2. When it disseminates to the CNS, it can cause meningoencephalitis, h/a, lethargy, altered mental status.  This is more common among those immunocompromised.
  11. How do you treat Cryptococcus species?
    • 1. Anti-fungal:
    • Start with Amphotericin B + Flucytosine;
    • Fluconazole for suppression of cryptococcosis.
  12. How do you prevent C. neoformans?
    Immunocompromised people should avoid areas of high bird droppings and birds in general.
  13. What is the life-cycle of Cryptococcus species?
    • 2 stages: 
    • Asexual: the budding basidiospore form.
    • Sexual: only seen in the lab; conjugation.
  14. What is the organism that causes tape worm in humans after ingesting infected pork?
    T.solium
  15. Describe the lifecycle of T.solium
    • The tapeworm has 2 stages:
    • 1. Sexual reproduction in the definitive host (humans)
    • 2. Asexual reproduction in the intermediate host (swine + humans)
  16. What is the transmission path of T.solium?
    • 1. Pigs/cattle ingest the eggs + proglottids from the environment.
    • 2. Eggs hatch and penetrate the animals' intestines and makes it way to organs, such as muscles, brain, and eyes.  The oncospheres develop into cysticerci here.
    • 3. Humans consume infected undercooked meat and the cysticerci uses its scolex to attach to the intestines to develop into adult tape worm. Additionally, may travel lymphohematogenously to other organs.
    • 4. Egg production and proglottid segments released via human feces and ultimately to the environment again.
  17. What is the pathology of T.solium?
    The proglottids rupture within the host intestine, causing the larvae to migrate to tissue and causing cysticercosis.
  18. What are the clinical manifestations of T.solium?
    • GI issues: abdominal pain, loss of appetite, weight loss.
    • Cysticercosis: happens via autoinfection; cyst formation in the brain, eyes, and muscles. Neuorocysticercosis symptoms include headaches, dementia, dizziness, and seizures. It is the most common cause of acquired epilepsy in the developing world.
  19. How do you treat T.solium?
    How do you treat cysticercosis?
    • 1. Antiparasitic: Praziquantel
    • 2. #1 + corticosteroid --dying cysticerci may cause inflammatory response.
  20. How do you diagnose T.solium?
    How do you diagnose cysticercosis?
    • 1. The proglottids are visible in a stool sample.
    • 2. CT/MRI, biopsy or immunoblot.
  21. How do you prevent T.solium?
    COOK YOUR PORK CORRECTLY.
  22. When would anti-parasitic drug be ineffective for T.solium?
    When the cysts are already dead (calcified) within the body.
  23. What organism causes toxoplasmosis?
    T. gondii, an obligate intracellular parasite (sporozoan).
  24. What are the definitive and intermediate hosts for T. gondii?
    • Definitive host: domesticated cats; sexual reproduction occurs in this host.
    • Intermediate host: humans and other warm-blooded mammals; asexual reproduction occurs in these host.
  25. How is T. gondii transmitted?
    • 1. Handling cat feces in the litter box.
    • 2. Environment/gardening near cat feces.
    • 3. Bigger animals eating infected cats.
    • 4. Vertical transmission from mom to baby
    • 5. Blood transfusions (rare).
  26. What are the 3 stages of how T. gondii can exist?
    • 1. Trophozoite: rapidly dividing and invasive.  The tachyzoites look crescent shaped.
    • 2. Bradyzoite: slow dividing; resides in tissue cyst within body to evade immune response.
    • 3. Sporozoite: protected from environment by residing in the oocyte.
  27. What is the pathology of T.gondii?
    Ingested sporozoite --> intestinal cells --> GI proteases release free parasites --> mature tachyzoites that multiplies a lot --> continues multiplying in tissue cyst (bradyzoite) to avoid immune system --> ruptures when cell dies --> can invade monocytes --> dissemination.
  28. What are the clinical presentation of T. gondii?
    • -Mostly asymptomatic and very common.
    • -Self-limiting mono-like disease, fever, and lymphadenopathy.
    • -For immunocompromised, highly lethal.
    • -Congenital: stillbirth, abortion, neonatal disease that can present later in life.
  29. How do you diagnose T. gondii?
    • 1. Detection of specific T.gondii IgG, IgM, IgA
    • 2. PCR amniotic fluid
    • 3. See the parasite on a tissue section stain
    • 4. CT: for lesions in AIDS patients--encephalitis.
  30. How to you treat T. gondii?
    Anti-parasitic drugs, however these are only supportive since the tissue cysts are resistant.
  31. How do you prevent T. gondii?
    Hand washing after handling litter box, gardening outside, etc.
  32. Why do we not have an immune response to prions?
    Prions are neither virus nor bacteria.  It is an infectious protein that is very resistant to being killed.
  33. What types of diseases can be caused by prions? (animals + humans)
    • Scrapies: goats and sheep
    • BSE: cattle
    • CJD, vCJD, kuru, FFI, GSS: humans
  34. What is the pathology for prions?
    There is a post-translational change in the cellular protein PrPc --> PrPsc that causes it to change its shape from alpha helices to beta sheets. This allows the prion to spread and vacuolization of neurons to occur --> neuronal death.
  35. How do you diagnose for prions?
    • 1. CSF analysis
    • 2. Western blot for PrPsc
    • 3. autopsy
    • 4. protein assay
  36. What is the treatment for prion diseases?
    There is no treatment.
  37. How do you prevent prion diseases?
    • 1. Ban animal products in feed.
    • 2. Sterilize hospital equipment (latrogenic CJD)
  38. How does one acquire vCJD?
    By eating infected cow meat
  39. How does one acquire kuru?
    By ingesting infected human tissue
  40. What is the most common way to get CJD?
    • 1. sporadic via somatic mutation (most common)
    • 2. Latrogenic --via bad grafts, dirty electrodes
  41. How do you get FFI?
    It's genetics, and you die from insomnia and dementia.
  42. Describe the morphology of HIV
    • +ssRNA
    • enveloped
    • diploid
    • Has core viral enzymes:
    • RT - reverse transcriptase
    • PR - protease
    • IN - integrin
  43. Why would you get a negative Ab test early during HIV infection?
    There is a lag time where viremia>Ab but the person is still infectious.
  44. What are the 2 types of HIV, and which is more common?
    • HIV-1: more common; has many subtypes including M,N,O,P.
    • HIV-2: less common, primarily found in W. Africa.  Harder to detect but not as aggressive.
  45. How does the term quasispecies apply to HIV?
    • Within the same host, HIV can evolve due to:
    • 1. high mutation rate during replication
    • 2. Template switching due to being diploid
    • 3. high replication rate
    • = new variants formed within the host.
  46. What are some clinical manifestations of HIV?
    Neurologically: cognitive and behavioral symptoms such as--decline in memory, concentration, weakness and tremors.  Depression and dementia.
  47. HIV mechanism of pathology
    Kills CD4+ T-cells, making the body susceptible to opportunistic infections
  48. How do you diagnose HIV?
    • 1. immunoassay for IgM initially
    • 2. RT-PCR
    • 3. Western blotting
  49. How do you treat HIV?
    ART/HAART--because HIV mutates so fast, you want to inhibit as many targets as you can; such as the core viral proteins + adhesion
  50. How do you prevent HIV?
    • Safer sex
    • Less risky behavior
    • Screenings
    • Don't share needles
  51. What is the organism that causes syphilis?
    T. pallidum, a spirochete that is very infectious and has low antigenicity (doesn't really trigger immune response)
  52. What are the stages of syphilis, and the clinical presentations involved?
    • Primary: lesion that heals
    • Secondary: rash that heals; systemic infection with variable lesion manifestations. Latency some time around here
    • Tertiary: focal lesions with that can cause neurosyphilis and damages to the parenchyma of the brain and spinal cord
  53. How is syphilis transmitted?
    • 1. sexual contact with infectious lesions
    • 2. vertical transmission
    • 3. blood product transfusion
  54. How do you diagnose syphilis?
    • -Don't culture it, it's too slow
    • -Serology test
    • -Analysis of CSF --especially if the eye or brain is involved or it's in the tertiary stage, or patient is HIV+.
  55. How do you treat syphilis?
    It is sensitive to PCN--which is also why you don't see many tertiary cases in the U.S
  56. How do you prevent syphilis?
    • Safe sex
    • Don't come into contact with the lesions
  57. What is the morphology of rhabdovirus (rabies)
    • -Bullet shaped
    • -Enveloped
    • -ssRNA
    • -Brings its own RNA-dep-RNA-pol
  58. How is rabies usually transmitted?
    • Bite
    • Saliva
    • Contact with infected nervous tissue
  59. What is the pathology of rabies?
    Rabies virus replicates at the site of inoculation - muscle/CT --> enters peripheral nerves --> CNS --> ENCEPHALITIS --> peripheral nerves --> disseminates.
  60. What are the clinical presentation of rabies?
    • Initially: fever, headache, weakness, discomfort
    • Later on: insomnia, agitation, hydrophobia, hypersalivation --> death in a few days.
  61. How do you diagnose rabies?
    • 1. Presence of negri bodies/cytoplasmic inclusion
    • 2. RT-PCR
    • 3. CSF for antibodies
    • 4. Skin biopsy at site of bite
  62. How do you treat rabies?
    If rabies is suspected, give post-exposure anti-rabies vaccine.
  63. How do you prevent rabies?
    Pre-exposure anti-rabies vaccine for spelunkers and vets.
  64. What disease must you have had in order to get SSPE? (subacute sclerosing panencephalitis)
    Measles --usually wild-type and not from vaccine
  65. When does SSPE usually appear?
    7-10 years after initial measles infections
  66. What are the stages of SSPE?
    • Stage 1: Treatable at this stage; impaired memory, abnormal behavior, myoclonic spasms and jerks.
    • Stage 2: Increased intensity of spasms and mental deterioration
    • Stage 3: Decline in body function, blindness, mute, comatose.
  67. What is the pathophysiology of SSPE?
    • It is a degenerative CNS disease characterized: 1. Change in personality --> convulsions --> dementia --> death.
    • 2. Diffuse encephalitis with sclerosing inflammation of gray and white matter.
    • 3. Presence of viral nucleocapsid in the cytoplasm of neurons and glial cells. No envelope = no immune response
  68. How do you treat SSPE?
    Antivirals: Ribavirin + interferon
  69. What causes PML and what does it affect?
    (Progressive multifocal leukoencephalopathy)
    JC virus; Demyelinates the white matter
  70. What is the pathophysiology of PML?
    Inhalation of virus causes infection in the tonsils --> travels to the kidneys and bone marrow where it remains latent --> reactivation --> neuroinvasion by crossing blood-brain barrier via B-cells --> infects oligodendroglia.
  71. Who is susceptible to PML?
    immunocompromised individuals
  72. Describe aseptic meningitis?
    • 1. Usually associated with virus, but is not always caused by a virus.
    • 2. Presence of mononuclear pleocytosis
  73. What are some causes of viral meningitis?
    • MEHH
    • 1. Enteroviruses
    • 2. HIV
    • 3. Herpesvirus
  74. What are some causes of viral encephalitis?
    • HHAIR-E
    • HIV
    • Herpesvirus
    • Arbovirus
    • Influenza
    • Rhabdovirus
  75. What are positive Kernig's and Brudzinski tests indicative of?
    Meningitis
  76. Describe latency
    • 1. All herpesvirus establish latency.
    • 2. Circularizes its genome
    • 3. Resides in the sensory neuron where immune response is lacking.
    • 4. Silences all lytic gene expression, expresses only LAT (latency assoc. transcript) to suppress viral replication
    • 5. Blocks apoptosis
    • 6. Reactivation occurs upon immune stress.
  77. Compare reservoir v. vector
    • Reservoir: the source of infection; infects the vector.
    • Vector: what transports/transmits the agent.
  78. Yellow Fever Virus (Flavivirus)
    Clinical signs
    Most are asymptomatic or have mild systemic symptoms. 15% progress to severe symptoms including: hemorrhagic fever, jaundice, bleeding, shock, and multiple organ failure.
  79. Yellow Fever Virus
    Pathogenesis
    Vector = mosquito --> replicates in lymph nodes and infects dendritic cells --> liver --> degradation of cells (presence of necrotic mass) --> release of cytokines.
  80. Yellow Fever Virus
    Diagnosis
    • Clinical diagnosis--location is tropical and subtropical S. America + Africa.
    • RT-PCR
    • Blood culture (1-4 wks)
    • Serology test
    • Liver biopsy
  81. Yellow Fever Virus
    Treatment and prevention
    • No treatment, just relief of symptoms.  
    • There is a vaccine.
  82. Dengue Fever (Flavivirus)
    Clinical signs
    • Mild fever --> high fever, severe headache, pain behind eyes, muscle and joint pains.
    • DHF: dengue hemorrhagic fever--lethal in children: fever, abdominal pain, vomiting, bleeding.
  83. Dengue Fever
    Pathogenesis
    Vector: A.aegypti mosquito that bites human host.  Viral replication takes place in dendritic cells --> immune response.
  84. Dengue Fever
    Diagnosis
    • Clinical signs
    • Immunoassay
  85. Dengue Fever
    Treatment
    No treatment; relief of symptoms
  86. Dengue Fever
    Prevention
    • Vector control
    • Remove stagnant water
    • Wear protective clothing
    • For DFH: maintain body fluid volume
  87. West Nile Virus (Flavivirus)
    Clinical symptoms
    • Most are asymptomatic
    • Febrile flu-like symptoms in 20%
  88. West Nile Virus
    Pathology
    • Vector: mosquito
    • Reservoir: wild birds
    • Bites humans and replicates at site of inoculation --> lymph nodes --> blood --> CNS --> affects neurons + immune-mediate tissue damage
  89. West Nile Virus
    Treatment
    No specific treatment.
  90. West Nile Virus
    Prevention
    • Use mosquito repellent
    • Wear protective clothing
    • Eliminate mosquito breeding grounds
    • Vector control
  91. West Nile Virus
    Diagnosis
    • Clinical symptoms--is it the summer time?
    • Serology testing of blood/CSF
    • Immunoassay
  92. Colorado Tick Fever Virus (CTFV) Reovirus Western, NW states
    Clinical symptoms
    • Febrile illness is the most common--fever, chills, headaches, pain behind eyes.
    • 2 stages of fever: 2nd stage is high fever + increased symptoms.
  93. CTFV
    Pathology
    • Vector: wood tick
    • Hosts: squirrels, chipmunks, rabbits, deers
    • Bite at site --> lymph --> blood --> CNS
  94. CTFV
    Diagnosis
    • Clinical signs
    • Blood work: virus can live in blood for 6 months
  95. CTFV
    Treatment
    No specific treatment, but remove the tick if still attached.
  96. CTFV
    Prevention
    • Don't go hiking or camping in the Rocky Mtns. 
    • It is seasonal and occurs mostly during the summer.
    • Avoid tick-infected areas
    • Wear proper attire if you must hike.
  97. California Encephalitis Virus Group (CEV) Bunyavirus (Midwest, SE states)
    Clinical symptoms
    • Children: fever, drowsiness, lack of mental alertness + orientation. Encephalitis, seizure in 50% of children affected.
    • Adults: asymptomatic, mild fever.
  98. CEV
    Pathology
    • Vector: mosquito A. triseriatus
    • Reservoir: chipmunks, squirrels, rabbits
    • Spreads the same way all the other viruses spread.
  99. CEV
    Diagnosis
    Serology
  100. CEV
    Treatment
    Symptom management
  101. CEV
    Prevention
    Same prevention as other mosquito viruses
  102. St. Louis Encephalitis Virus (SLEV) East + Central US (Flavivirus)
    Clinical symptoms
    • Most are asymptomatic or have headache and fever.
    • Severe encephalitis can occur
  103. SLEV
    Pathology
    • Vector: mosquito
    • Reservoir: wild birds
    • Dead-end host: humans
    • Same way other virus infections occur
  104. SLEV
    Treatment
    Treat symptoms
  105. SLEV
    Diagnosis
    • Clinical findings
    • Serology
    • CSF analysis
  106. SLEV
    Prevention
    Mosquito prevention stuff
  107. WEST (west of MS) + EAST (Atlantic + gulf) equine encephalitis virus (EEEV, WEEV) Togavirus
    Clinical symptoms
    Ranges from flu-like to encephalitis, coma and death
  108. EEEV/WEEV
    Pathology
    • Vector: mosquito
    • Reservoir: small birds
    • Dead-end host: humans and horses
    • Spreads the same way other viruses spread
  109. EEEV/WEEV
    Diagnosis
    Blood test/ CSF analysis
  110. EEEV/WEEV
    Treatment
    Treat the symptoms
  111. EEEV/WEEV
    Prevention
    Mosquito related prevention--EEEV has a higher mortality + morbidity than WEEV.
  112. What is the pathology for arboviruses?
    bite --> replication at site --> viremia --> spreads via blood and lymph to other organs depending on tropism --> immune response --> inflammation + necrosis
  113. How do you treat most arboviruses?
    Treat the symptoms only
  114. How do you prevent arboviruses?
    • Eliminate or control the vector
    • Wear protective clothing
  115. HSV-1/2
    Clinical signs
    • HSV-1: mostly children, fever, headache, mouth sores and lesions, lymphadenopathy.
    • HSV-2: genital sores
  116. HSV-1/2
    Pathology
    It is ubiquitous and host-adapted. Transmitted via close contact and inoculation into susceptible mucosal surfaces.
  117. HSV-1/2
    Diagnosis
    • Cell culture to observe for cytopathic effect (Cowdry cells)
    • PCR the CSF to diagnose encephalitis and meningitis.
  118. HSV-1/2
    Treatment
    Anti-viral: acyclovir/foscarnet to inhibit viral DNA polymerase. IV version to treat HSV encephalitis and neonatal diseases. This only decreases duration but doesn't cure or stop the virus shedding. Has no effect on latent infection.
  119. HSV-1/2
    Prevention
    • Safe sex
    • Don't touch the lesions
  120. What should you know about non-polio enterovirus?
    • 1. Infects GI tract, prefers low pH
    • 2. Transmission via fecal-oral route, blister, childbirth, and indirect transmission.
    • 3. Resistant to most disinfectant, but sensitive to formaldehyde and bleach
    • 4. No vaccine and specific treatment
    • 5. Hand-washing is the best prevention
    • 6. Disease manifestation: due to virus-induced cell lysis.
  121. Coxsackievirus A/B (enterovirus)
    Clinical symptoms
    • A: HMFT sores
    • B: Pleurodynia and chest inflammation
  122. Coxsackievirus A/B
    Pathology
    Transmission via fecal-oral route and respiratory aerosols.  Virus replicates in URT and distal small bowel.  It then disseminates to other sites.
  123. Coxsackievirus A/B
    Diagnosis
    • Clinical features--blisters
    • RT-PCR
    • Serology test
  124. Coxsackievirus A/B
    Treatment
    Non-specific treatment
  125. Coxsackievirus A/B
    Prevention
    • Tell your children:
    • Wash hands
    • Avoid going from fecal to oral route 
    • No vaccine

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