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Unit 4: D & D > Common Viral Pathogens I > Flashcards

Common Viral Pathogens I Flashcards

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1
Q

What does HSV1 stand for?

A

Herpes simplex virus type I

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2
Q

HSV1 target cell type?

A

mucosal epi

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3
Q

HSV1 latency?

A

neuron (ganglia)

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4
Q

HSV1 transmission?

A

close contact

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5
Q

HSV1 clinical manifestations?

A

orofacial lesions, some genital lesions, encephalitis, herpes whitlow, herpes keratitis, neonatal herpes

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6
Q

HSV1 virus type?

A

ds DNA virus

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7
Q

HSV1 incubation period?

A

2-12 days (4 on avg)

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8
Q

What is the primary infection of HSV1?

A

first infection; usu asymptomatic; if symptoms present, they’re stronger than later; no antibody present

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9
Q

What is the HSV1 latency period?

A

when virus is dormant in the body; on trigeminal ganglion in facial disease; on sacral ganglion in genital disease; waits in the nucleus

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10
Q

What is the HSV1 reactivation phase?

A

virus emerges from latency and begins to replicate again

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11
Q

What are the signs/symptoms during the HSV1 reactivation phase?

A

orofacial, cornea (keratitis), or perineal (genital) lesions; triggered by variety of events; reactivation commonly asymptomatic or less severe than 1a infection

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12
Q

Why is herpes often spread unknowingly?

A

sometimes it’s asymptomatic during shedding phase, or the lesions are so small and trivial that they go unnoticed

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13
Q

What is gingivostomatitis?

A

symptomatic primary infection from HSV1; ulcers on gums, lips, and tongue (anterior); drooling; fever; lip and cervical lymph node swelling

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14
Q

What is herpetic whitlow?

A

transfer of virus from mouth to fingers via cuts or abrasions; erythema, swelling, and grouped vesicles that grow into pustules with cloudy fluid; tender to the touch

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15
Q

What is genital herpes?

A

usually HSV2 infection but HSV1 30% of the time; painful vesicles and ulcers in genital and perianal region that last 10-14 days; swelling; painful urination

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16
Q

What is herpes keratitis?

A

HSV infection of the cornea, usually by HSV1; produces dendritic lesions of the cornea that can cause scarring and blindness (one of the leading causes)

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17
Q

What is encephalitis?

A

herpes infection of the brain; 1a or reactivation; bloodborne or neuronally spread; fulimant, hemorrhagic, necrotizing; usu temporal lobes; altered mental status and death results

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18
Q

What is neonatal herpes?

A

primary infection of a neonate acquired en utero, peripartum (most often), or postpartum; mostly HSV2

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19
Q

What is the most common reactivation of HSV1?

A

herpes labialis (cold sores)

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20
Q

1a infection of any of the 3 branches of cranial nerve 5 (____, _____, or _____) leads to latent infection of nerve cells in the trigeminal ganglion.

A

ophthalmic, maxillary, mandibular

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21
Q

1a infection of any of the 3 branches of cranial nerve 5 (ophthalmic, maxillary, mandibular) leads to latent infection of nerve cells in the ______.

A

trigeminal ganglion

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22
Q

1a infection of any of the 3 branches of cranial nerve ____ (ophthalmic, maxillary, mandibular) leads to latent infection of nerve cells in the trigeminal ganglion.

A

five

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23
Q

Members of the ______ family all contain a ds-DNA genome that is protected by an icosahedral capsid and a glycoprotein-rich envelope.

A

Herpesviridae

24
Q

Name the 3 viruses in the alpha subfamily and where they establish latency.

A
  1. HSV-1
  2. HSV-2
  3. VZV
    sensory ganglia
25
Q

Name the 3 viruses in the beta subfamily and where they establish latency.

A
  1. CMV
  2. HHV-6
  3. HHV-7
    monocytes and lymphocytes
26
Q

Name the 2 viruses in the gamma subfamily and where they establish latency.

A
  1. EBV
  2. KSHV
    B cells
27
Q

How does herpesvirus enter the cell?

A

binds to cell surface proteins, fuses to cell membrane, releases nucleocapsid into membrane where it travels to nucleus along microtubules

28
Q

How is herpesvirus replicated?

A
  1. synthesis of intermediate early (IE) genes
  2. express early (E), which include DNA pol, thymidine kinase (TK), helicase
  3. express L genes, which encode structural proteins (capsids and glycoproteins)
29
Q

Where do herpesviruses obtain their envelopes?

A

from the Golgi

30
Q

Members of the Herpesviridae family all contain a ____ that is protected by an icosahedral capsid and a glycoprotein-rich envelope.

A

ds-DNA genome

31
Q

Members of the Herpesviridae family all contain a ds-DNA genome that is protected by _____ and a _____.

A

an icosahedral capsid; glycoprotein-rich envelope

32
Q

What is the most common event in herpesvirus reactivation?

A

it’s asymptomatic, but viruses are shed

33
Q

What does VZV stand for?

A

varicella zoster virus

34
Q

VZV causes 2 clinical syndromes, ____ and ____.

A

Chickenpox (varicella); shingles (zoster)

35
Q

Why is Chickenpox in pregnancy bad?

A

prego fem at high risk for developing varicella pneumonia and death

36
Q

What are the s/s of chickenpox?

A

fever, headache, malaise; rash appearing in crops or waves that starts on face or trunk and spreads to extremities; vesicles to pustules that rupture and scab at all different times over 7 days

37
Q

Pathogenesis of chickenpox?

A

enters via respiratory tract, spreads to lymphoid system where it replicates for 2-4 days. 1a viremia for 4-6 days, then the virus replicates in the liver and spleen. 2a viremia follows and spreads to skin where rash develops 14-16 days after exposure.

38
Q

Name 6 chickenpox complications.

A
  1. 2a infection/cellulitis (group A strep infection of skin)
  2. pneumonia (bacterial from group A strep or viral in prego women or immunocompromised)
  3. necrotizing fasciitis (infection into the fascia that shears off nerve endings and blood supply from group A strep)
  4. encephalitis/encephalomyelitis (CNS infection via cross-reacting antibodies in immunocompromised)
  5. hepatitis (immunocompromised)
  6. congenital varicella syndrome (organ and tissue abnormalities in developing fetus when mom has chickenpox in 8th-20th week)
39
Q

How is varicella treated?

A

usually none, but can give acyclovir; also live attenuated vaccines

40
Q

How does VZV reactivate?

A

it tracks down the sensory nerve to the skin along a dermatome where it causes necrosis and inflammation of neurons

41
Q

____ is the only herpesvirus that does not exhibit asymptomatic viral shedding.

A

VZV

42
Q

How is VZV shed in shingles?

A

only from the shingles lesions

43
Q

What are the s/s of Shingles?

A

radicular pain preceding grouped vesicles on an erythematous base confined to a single dermatome that do not cross the midline

44
Q

Name 3 ways to diagnose shingles (aside from clinically).

A
  1. direct fluorescent Ab
  2. VZV PCR
  3. viral culture
45
Q

What is the treatment for shingles?

A

acyclovir and analgesics; Zostavax vaccine

46
Q

VZV is the only herpesvirus that does not exhibit ____.

A

asymptomatic viral shedding

47
Q

What is congenital CMV?

A

babies born to mothers with a 1a CMV infection

48
Q

What are the s/s of congenital CMV?

A

low birth weight, microcephaly, hearing loss, mental impairment, hepatosplenomegaly, skin rash (blueberry muffin) due to extramedullary hematopoiesis of the skin, jaundice, chorioretinits

49
Q

What will be the serology test results in an acute primary CMV infection?

A

CMV IgM positive, IgG negative

50
Q

What will be the serology test results in a pt that has never had a CMV infection?

A

negative IgM, negative IgG

51
Q

What will be the serology test results in a pt that has had a CMV infection sometime in their life?

A

negative IgM, positive IgG

52
Q

What will be the serology test results in a CMV reactivation?

A

positive IgM, positive IgG

53
Q

What is the distinctive cytological finding in CMV?

A

owl’s eyes- dense, dark nuclear body surrounded by a halo in infected cells

54
Q

What is the treatment for CMV?

A

usually none needed; immunocompromised get Ganciclovir or CMV-IG

55
Q

How do T cells play a role in VZV?

A

lowered T cell immunity to varicella puts people at risk for shingles

Unit 4: D & D (22 decks)

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