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Microbiology Exam 2 > Neurotropic Agents > Flashcards

Neurotropic Agents Flashcards

1
Q

List the 5 viruses discussed

A
  1. HSV encephalitis
  2. Rabies virus
  3. West Nile virus
  4. Enteroviruses
  5. Spongiform encephalopathies
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2
Q

Define encephalitis, meningitis and aseptic meningitis.

A
  • encephalitis: infection of brain parenchyma
  • meningitis:infection of meninges
  • aseptic meningitis: viral infection of meninges
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3
Q

Define myelitis, encephalomyelitis, and meningoencephalitis

A

myelitis: infection of spinal cord
encephalomyelitis: infection of brain and spinal cord
meningoencephalitis: infection of brain and meninges

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4
Q

Neurotropism and neurovirulence

A
  • NT: ability of an infectious agent to infect cells of the nervous system
  • NV: potential to cause disease once within the nervous system
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5
Q

Blood-brain barrier is due to meninges and the endothelial cells extremely tight junctions. Give 4 impacts of this barrier.

A
  1. barrier to entry of infectious agents
  2. barrier to protective components of the immune response like antibodies, complement, inflammatory cells
  3. barrier to penetration of antimicrobial drugs
  4. restrictive nature of intracranial and intravertebral spaces leading to increase in pressure during swelling and inflammation
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6
Q

2 ways to gain entry into the CNS

A
  1. hematogenous route: infect endothelial cells, enter at choroid plexus due to no tight junctions, migration of infected inflammatory cells
  2. neural route: anterograde movement in axons from site of infection; olfactory nerve endings which is only CNS in direct contact with environment
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7
Q

Clinical signs of encephalitis

A
  • acute onset of febrile illness with headache and altered mental status
  • KEY: early mental status changes, can be focal or diffuse
  • more commonly due to viruses
  • behavioral or speech problems, neurological signs, seizures
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8
Q

Most common causes of sporadic and epidemic encephalitis

A
  • sporadic: HSV

- epidemic: WNV

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9
Q

Differences in symptoms between encephalitis and meningitis

A

-encephalitis is less likely to have fever, more likely to have personality/behavior changes

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10
Q

Meningitis clinical signs

A
  • classic triad: fever, headache (severe, frontal, photophobia), neck stiffness
  • can have altered mental status
  • symptoms usually appear rapidly and may include nausea and vomiting
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11
Q

3 signs to test for meningitis

A
  1. Jolt accentuation: tear head rapidly, does HA increase?
  2. Kernig sign: one leg with hip flexed, pain in back with extension of knee
  3. Brudzinski sign: flexion of legs and thighs when neck is flexed
    * *idea is to stretch the meninges, and if meningitis is present, there will be inflammation around the nerve roots and this causes pain upon stretching. Specific, not sensitive
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12
Q

Aseptic meningitis: what is it? most common viruses causing it?

A
  • inflammation of meninges without involvement of the brain due to a viral infection
  • enteroviruses (echo and coxsackie), HSV-2, Mumps (rarely)
  • usually self-limited unless parenchyma becomes involved and it turns into meningoencephalitis
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13
Q

What can be used to identify what virus is responsible for meningitis?

A

-PCR from CSF

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14
Q

Compare CSF cell type, protein levels, glucose levels, gram stain, and pressure between bacterial vs. viral meningitis

A
  • bacterial: PMNs, increased protein, decreased glucose, 60% gram stain +, increases pressure
  • viral: lymphocytes, normal protein levels, normal to slight decrease in glucose, negative gram stain, normal pressure
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15
Q

How does one treat HSV encephalitis?

A
  • acyclovir immediately, IV, for 14-21 days

- detect viral DNA in CSF

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16
Q

HSV encephalitis: how will it look on an MRI?

A

-fronto-temporal lesions

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17
Q

Rabies virus: family and structure. What animals to be aware of in US.

A
  • rhabovirus
  • negative-stranded RNA
  • enveloped
  • NON-segmented
  • raccoons> skunks> bats> foxes
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18
Q

T/F: almost any mammal can be infected with rabies.

A

-true

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19
Q

What is the most common vector for human rabies? Why does this cause many cases to miss preventative immunization?

A
  • bats in US, dogs in other countries

- exposure was not recognized because the bat bite was too small or because there was no bite at all

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20
Q

2 types of rabies virus spread

A
  1. centripetal: from muscle, through nerve, to CNS; site of inoculation influences time to symptoms
  2. centrifugal: from CNS to cornea and salivary glands (sets up for transmission)
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21
Q

What do we expect to see in rabies-infected neurons in CNS?

A

-negri bodies and lymphocyte infiltration

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22
Q

Symptoms of rabies

A
  • long and variable incubation period without symptoms, usually 4-6 weeks
  • prodrome phase with malaise, fever, headache
  • neurologic phase with anxiety, confusion, agitation with delerium, spasms, and hydrophobia
  • coma then death
  • nearly always fatal once symptoms arise
23
Q

Explain the hydrophobia with rabies

A

-fear of water due to difficulty in swallowing

24
Q

When to treat rabies: 1. bit by dog, cat, or ferret

2. skunks, bats, raccoons, foxes 3. liverstock, rodents

A
  1. if animal is available, observe it for 10 days and if no sx, don’t treat; if rabid or suspected, treat immediatey
  2. regard as rabid unless proven otherwise and treat
  3. almost never require post-exposure prophylaxis
25
Q

What type of vaccine is the rabies vaccine?

A

-killed, inactivated vaccine

26
Q

Rabies treatment post-exposure in immunized vs. non-immunized person

A
  • non-immunized: wound cleanse, RIG full dose, vaccine

- immunized: wound cleanse, NO RIG, vaccine

27
Q

What family does West Nile virus belong to? what are others in this same family? describe its structure and transmission

A
  • flavivirus along with yellow fever, dengue, japanese encephalitis
  • spread by mosquitos between animal hosts (birds) and humans
  • enveloped, icosahedral, positive ssRNA
28
Q

Flaviviruses are major causes of ______________.

A
  • viral encephalitis

- but not all cause encephalitis (Dengue, Yellow fever, Hep C)

29
Q

What are the 2 flaviviruses of medical importance in the US?

A

-St. Louis and West Nile

30
Q

What is an arbovirus?

A

-a virus spread by biting insects, like West Nile

31
Q

When does WNV peak?

A

-late summer/early fall when mosquitos also peak

32
Q

Most WNV cases are asymptomatic and occur in what time frame? However, mild and severe cases can happen; describe the symptoms of these

A
  • most in late summer, early fall
  • Mild WN fever: 3-14 day incubation after bite, fever, HA, myalgia, anorexia, can have generalized lymphadenopathy and GI complaints, truncal maculopapular in some patients, last 3-6 days
  • Severe: WN Meningoencephalitis: fever, weakness, GI complaint, headache, fever, stiff neck, lower motor neuron disease, may be confused with GBS
33
Q

Who is at the highest risk of acquiring Severe West Nile Meningoencephalitis?

A

-advanced age

34
Q

Polio: what family does it below to and describe its structure

A
  • picornaviridae

- nonenveloped, positive sense ssRNA

35
Q

2 classes of illness human EV cause and which they more commonly cause.

A
  • aseptic meningitis: 85-90% of CA cases

- encephalitis (10-20% of acute encephalitis)

36
Q

3 ways to describe what kind of “virus” Polio is.

A
  1. enterovirus
  2. pantropic virus: plasma viremia
  3. neutrotropic virus: invades CNS
37
Q

How is Polio transmitted? and describe it’s pathogenesis.

A
  • transmitted via hand-to-hand to mouth
  • ingested
  • replicates in tonsil and peyer’s patches
  • excreted in throat and feces
  • hands contaminated
38
Q

Describe Polio’s pathogenesis as a neutropic virus

A
  • invades CNS
  • localizes in ANTERIOR HORN CELLS
  • both necrotic and apoptotic
  • lower motor neuron paralysis without sensory loss
39
Q

_________ % of polio infections are asymptomatic.

A
  • 90%

- 1-2% get aseptic meningitis and less than 1% get paralytic polio

40
Q

2 types of polio vaccines and what they induce.

A
  • Live oral polio vaccine (OPV) called Sabin vaccine. Taken orally once, induced IgA secretion in gut which protects from wild-type virus infection. It replicates, is shed, and can infect (immunize) others. Highly effective, but at a LOW rate, virus mutates and become virulent, and can cause paralytic polio
  • Inactivated polio vaccine (IPV): Salk vaccine. Induces antibodies, protects the CNS. Safer due to no risk of reversion, but dont not protect gut as well as OPV, takes 4 doses, and is not shed so not bystander effect*used in US
41
Q

How many types of polio exist and are any eradicated?

A
  • 1,2,3

- 2 is eradicated

42
Q

What is another name for transmissble spongioform encephalopathies? Describe where they infect and what they do.

A
  • Prions
  • degenerate disorders of the brain
  • spongioform degeneration and astrocytic gliosis
  • long incubation time of many years
  • invariably fatal
  • incubation time indicated barrier
43
Q

What does prion lack?

A
  • nucleic acid

- it is just a protein!!

44
Q

What causes spongioform encephalopathies? What does disease result from?

A
  • prions

- aberrant folding of a single protein called the prion protein, PrP

45
Q

There is a prior protein in all mammals and each tends to cause disease in its specific host. Prion diseases can be transmitted between species by incolulation or dietary exposure, but transmission is far more efficient _________.

A

-when it occurs within species

46
Q

What is the name of spongioform encephalopathy in humans? Describe symptoms.

A
  • Creutzfeldt-Jakob-Disease (CJD)
  • progressive dementia over months, insomina fatugie, visual symptoms including cortical blindness, startle myoclonus, ataxia, seizures, abnormall EEG
  • NO FEVER SYSTEMIC SIGNS BECAUSE NOT AN INFECTION
47
Q

Spongiform lesions are related to what?

A

-deposits or fibrils of PrPsc in brain

48
Q

What is infectivity of PrPsc resistant to? What is it sensitive to?

A
  • heat
  • nucleases
  • X-rays, UV
  • SENSITIVE TO PROTEASES= PROTEIN
49
Q

PrPc and PrPsc are biochemically the same, but they are _________.

A
  • folded differently (normal is alpha-helical and abnormal is beta sheets_
  • prion diseases result from misfolding of prion protein
50
Q

Can PrP knockout mice get spongioform disease?

A
  • no

- in fact, they are normal without protein at all so its function is unknown

51
Q

3 ways to get CJD and which is the most common?

A
  • iatrogenic CJD: infection from prion contaminated grafts
  • sporadic CJD: somatic mutation or spontaneous conversion to PrPsc* Most common
  • familial CJD: inherited gene mutation
  • variant CJD: infection from bovine prions
52
Q

Mad Cow disease

A
  • bovine spongioform encephalopathy (BSE)
  • classic spongioform encephalopathy that is linked to contaminated feed ingredients and spread to humans eventually
  • variant CJD
53
Q

vCJD vs. classical (sporadic/familial) CJD

A

-variant: mostly young people; different symptoms, tissue distribution, and neuropath from classical CJD

54
Q

What is the gold standard for diagnosing CJD?

A

-neuropathology exam

Microbiology Exam 2 (11 decks)

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