Micro: Greenberg 3 Flashcards

1
Q

What are the clinical hallmarks of encephalitis?

A

confusion, disorientation, acute changes in ideation and thought

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2
Q

What will CSF exam of viral meningitis show?

A

elevated WBC, usually w mononuclear pleocytosis of lymphocytes, normal or elevated protein, normal glucose

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3
Q

What is the microbiology of enteroviruses?

A

small nonenveloped RNA called picornaviruses
includes coxsackie A & B, echovirus, polio, enterovirus 71 (brainstem encephalitis)
humans only natural hosts, most common cause of viral meningitis

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4
Q

How are enterviruses spread?

A

fecal oral - poor hygienic environments, day care
resistant to pH, detergents and disinfectants, heat and sewage treatment
household spread common
most common in SUMMER (jun-Oct)

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5
Q

How is enterovirus diagnosed? Treated?

A

PCR
most resolve spontaneously, only few have sequelae, no current treatment or vaccine
maybe ISG for neonates and immunocompromised, interferon alpha

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6
Q

What are the clinical manifestations of enterovirus?

A

non-specific febrile illness, respiratory illness, hematologic conjunctivitis, herpangina (mouth blisters), hand-foot-mouth syndrome, pleurodynia, myocarditis, meningitis, encephalitis, congenital/neonatal inf

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7
Q

What is HSV type II meningitis?

A

sexually transmitted

pts have typical presentation and lab findings of viral meningitis

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8
Q

What is Mollaret’s meningitis?

A

benign recurrent aseptic meningitis - symptoms resolve w/i 5 days and pt recovers without sequelae
LP consistent w viral meningitis
mostly caused by HSV2 - only minority have genital herpes
prophylactic acyclovir

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9
Q

Which types of transmission/syndromes are caused by which type of HSV?

A

HSV type 1 = encephalitis, respiratory

HSV type 2 = meningitis, sexually transmitted

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10
Q

How is HSV encephalitis diagnosed?

A

mostly in temporal lobe

CSF PCR - false negative if hemoglobin or other inhibitors present –> repeat PCR 1-3 days later

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11
Q

What are the four main clinical syndromes of poliomyelitis?

A

asymptomatic: viral replication limited to oropharynx and gut
minor illness: nonspecific febrile illness, headache, malaise, sore throat, usually prompt resolution
nonparalytic aseptic meningitis: resolves w/o seqeulae
secondary viremic spread to nervous system –> flaccid paralysis

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12
Q

What is the diagnosis/treatment/prevention of polio?

A

CSF findings of aseptic meningitis
no antiviral therapy - maintain fxn
2 types of vaccine - live attenuated (IgA and GALT but not used anymore) and killed (only IgG)

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13
Q

What is the cycle of HSV-1 inf causing HSE?

A

after acute inf causes latent in trigeminal ganglion - reactivates and replicates - some fibers innervate meninges adjacent to temporal lobe

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14
Q

What is the virology of west nile virus?

A

member of flavivirus family
+sense ssRNA
belongs to japanese encephalitis virus group - St. Louis also a member

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15
Q

When does St. Louis encephalitis cause disease?

A

late summer and early fall - dz primarily in older people

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16
Q

What are the clinical manifestations of St. Louis encephalitis?

A

coarse tremors (inv of substantia nigra)
muscular weakness rare
transient parkinson like tremor

17
Q

How is St. Louis encephalitis/WNV diagnosed?

A

serologically off blood and CSF, demonstrate presence if IgM

18
Q

What are the clinical syndromes associated w WNV?

A

vast majority just have asymptomatic or febrile syndrome
neuroinvasive = meningitis, ecephalitis, meningoencephalitis, or polio-like syndrome
older individuals affected predominately, acute flaccid paralysis

19
Q

What clinical manifestations help distinguish WNV from St. Louis encephalitis?

A

tremor if basal ganglia involved but mild and in minority in WNV
muscular weakness profound in WNV

20
Q

What are factors involved in neurotropic WNV?

A
upregulation of genes involved in IFN signalling, T cell recruitment, MHC class I and II antigen presentation, apoptosis
HTN and vascular dz may predispose
21
Q

What is the vector control for WNV?

A

aerosols don’t affect aquatic stages of mosquitos
mortality restricted to “adults” in flight
graded drainage systems
fix poorly constructed apts

22
Q

What is the treatment and prevention for WNV?

A

no effective vaccines for humans or antiviral agents
looking for protease inhibitors
MyD88 inhibits by inhibiting replication in subset of cells
vaccine for horses

23
Q

What kind of virus is the rabies virus?

A

RNA rhabdovirus

24
Q

What is the cycle of the rabies virus once it enters the body?

A

binds to peripheral nerves - spreads retrograde back up to the brain - affects hippocampus, brainstem, pons, Purkinje cells of cerebellum - disseminates along nerves to salivary glands and other cells

25
Q

What is the clinical progression/stages of inf with rabies?

A

incubation period - most variable in length
prodromal phase - fever, lethargy, vomiting, anorexia, headache, pain at bite - 2-10 days
neurological stage - loss of coordination, paralysis, delirium, confusion (hypersalivation, hydrophobia)
coma and death - almost invariably fatal

26
Q

How is rabies diagnosed?

A

late, viral antigen in CNS
can be isolated and cultured but only after neurological dz
brain biopsy - Negri body = intracytoplasmic inclusions of viral nucleocapsid

27
Q

What are the two cycles of reservoirs of rabies? the two forms?

A

urban - dogs main transmitters
sylvatic - large number of hosts
encephalitic, paralytic

28
Q

What is the prevention of rabies?

A

vaccine - pre-prophylactic for high risk, prophylactic post-exposure - also give hyper-rabies immunoglobulin (HRIG) - *not effective once symptoms develop

29
Q

How is anti NMDA receptor encephalitis diagnosed?

A

mild CSF lymphocytic pleocytosis
T2 FLAIR hyperintensities
tumors often found

30
Q

What are the treatment and prognostic factors for anti NMDA receptor encephalitis?

A
most respond to immunotherapy (steroids, IVIG, plasmapheresis)
second line (rituximab, cyclophosphamide)
recovery can take up to 10 months, 3/4 do recover
31
Q

What is postinfectious encephalitis?

A

after viral inf (VZV), most commonly children, winter or spring
characterized by multi-focal perivenous demyelination (CD8 cells, autoimmune)
ADEM not consequence of specific inf or immunization
outcome usually favorable, 30% will develop MS

32
Q

What are signs and symptoms of postinfectious encephalitis?

A

meningeal signs
multi focal neurologic signs raise suspicion of ADEM
MRI w gadolinium enhancement

33
Q

What is the virology of JC virus and PML?

A
polyoma family (includes BK and SV40)
predominately in pts w advanced AIDs
related to papillomaviruses
34
Q

What is subacute sclerosing panencephalitis?

A

associated w prior measles inf
recover, then 6-15 yrs later progressive neurological degeneration
intact viral particles not present, but particles lacking M protein and viral nucleic acids detected
no treatment, usually death

35
Q

What is Reye’s syndrome?

A

encephalopathy (not encephalitis) associated with inf viral illness
influenza B and varicella mostly
has acute fatty liver
linked to use of aspirin