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Dermatology Board Prep > DERM (11) Infections, Infestations, and Bites > Human Herpesviruses > Flashcards

Human Herpesviruses Flashcards

1
Q

How many human herpes viruses that we need to know?

A

8 (HHV-1 through 8)

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2
Q

What type of virus is the human herpes virus?

A

Double-stranded DNA virus w/ a glycoprotein-containing envelope.

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3
Q

Where do the human herpes viruses replicate?

A

The host nucleus

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4
Q

What diseases do HSV1 and HSV2 cause?

A

Both cause recurrent vesicular eruptions. HSV1 is classically orolabial and HSV2 is classically genital although this is changing.

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5
Q

Where does the herpes virus remain dormant after primary infection?

A

In sensory nerve dorsal root ganglion

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6
Q

Risk factors for genital herpes?

A

Age 15-30 years, increased number of sexual partners, lower-income/educations, HIV + (also works in reverse, this increases the risk of HIV), MSM

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7
Q

How does HSV1/2 evade the immune system?

A

Decreases expression of CD1a by APC’s, decreased TLR receptor signaling.

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8
Q

What are some reactivation triggers for HSV?

A

Stress, UV (UVB>UVA), fever, injury (chemical peel or fractionated laser) and immunosuppression

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9
Q

Clinical appearance of HSV1/2

A

Grouped/clustered vesicles on a red base. Note that this can become pustules, erosions (look for scalloped borders due to coalescence), ulcers, and will ultimately crust over

Lasts about 6 weeks to completely resolve

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10
Q

What is the presentation of primary versus recurrent HSV1/2?

A

After 3 to 7 days postinfection–>prodromal sx’s (tender LAD, malaise, anorexia, and fever)–>mucocutaneous lesions. There can be pain, tenderness, tingling just before lesions erupt

  • Recurrent lesions are generally milder than primary infections. Can have a 24 hr prodrome of burning, itching, tingling
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11
Q

What is a key difference between herpangina and orolabial herpes infection?

A

Herpes tends to affect the buccal mucosa and anterior mouth (recurrent herpes tends to affect the vermillion border). Whereas, herpangina is the posterior mouth/pharynx

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12
Q

In which sex does primary genital herpes tend to be worse?

A

It is usually worse in women as they are more at risk for extragenital involvement. Watch for urinary retention and aseptic meningitis (10%).

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13
Q

How long does a recurrent episode of genital herpes last?

A

Approximately 1 week

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14
Q

What is the primary HSV infection like in genital herpes?

A

Often asymptomatic, but can have LAD, dysuria (more in women), painful/tender lesions on the external genitalia, vagina, cervix, buttocks, and perineum (women)

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15
Q

What is eczema herpticum and what disorders is it seen in?

A

It is a widespread, sometimes severe HSV infection on areas with skin barrier disruption. These disorders that increase the risk include: atopic dermatitis (namesake), Darier’s, Hailey-Hailey

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16
Q

What virus usually causes eczema herpeticum?

A

HSV-1, associated with Th2 shift in immune status

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17
Q

Atopic dermatitis risk factors for eczema herpeticum?

A

Severe atopic dermatitis, children with onset of AD <5 years old, increased IgE levels, increased eos, and food/environmental allergies

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18
Q

What is herpetic whitlow and what virus most commonly causes it?

A

It is HSV on the digits. HSV1 is more common in children and HSV2 is more common in adults

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19
Q

What is herpes gladiatorum and where does it normally present?

A

It is an HSV infection from athletic contact (wrestling, etc). It is most commonly seen on the face/neck and forearm (think areas with contact in sports)

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20
Q

What do we call it if we see herpetic vesicles in the beard area (follicular based)?

A

HSV folliculitis (herpetic sycosis)

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21
Q

What other surfaces must be considered for HSV infection in severely immunocompromised?

A

Can also involve the respiratory and GI tracts in the severely immunosuppressed

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22
Q

What is seen clinically in ocular HSV?

A

Keratoconjunctivitis w/ lymphadenopathy and branching dendritic corneal ulcer.

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23
Q

What herpes viruses are most common in ocular HSV?

A

HSV-2 in children, HSV-1 in all else

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24
Q

What part of the brain is most often affected in HSV encephalitis?

A

Temporal lobe

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25
Q

What gene mutations might be associated with getting HSV encephalitis?

A

TLR-3 or UNC-93B

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26
Q

How is a diagnosis of HSV made?

A
  • Viral culture: low sensitivity, high specificity
  • Direct fluorescent antibody assays, Western blot (gold standard)
  • PCR (most sensitive/specific)
  • Tzanck smear
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27
Q

What is the histology of HSV infections?

A

Look for intraepidermal vesicle with slate-gray enlarged keratinocytes from ballooning degeneration and viral changes of margination of the chromatin (most sensitive sign)

Can also see Cowdry A inclusion bodies which are eosinophilic inclusions in the nucleus

Will also see varying degrees of epidermal necrosis and infiltrate

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28
Q

Treatment for recurrent orolabial herpes?

A

Oral penciclovir/valacyclovir, topical penciclovir, or topical acyclovir/hydrocortisone comb

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29
Q

What is the treatment for recurrent genital HSV?

A

Oral acyclovir/famciclovir/valacyclovir.

  • Meds need to be given within 48 hrs of starting to decrease sx’s and viral shedding
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30
Q

Who receives suppressive daily medications for herpes infections?

A

Those patients have >6 outbreaks per year

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31
Q

In what settings would you consider IV acyclovir for an HSV1/2 infection?

A

Eczema herpeticum may need it, neonatal HSV, HSV in immunosuppressed patients

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32
Q

What medications can be given in cases of resistant HSV ( and who is at risk for resistant HSV)?

A

Foscarnet and cidofovir, immunosuppressed patients are more likely to have resistant HSV

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33
Q

What is the most common cause of Erythema multiforme minor?

A

HSV-1

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34
Q

What is a significant cause of death in patients with disseminated zoster?

A

SIADH

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35
Q

What is the primary and secondary forms of HHV-3/Varicella infection?

A

Primary = chicken pox (varicella)

Secondary= shingles (herpes zoster)

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36
Q

Who is most at risk of getting zoster/shingles?

A

The elderly and immunosuppressed, this also increases the risk for disseminated dz

Other risk factors: physical and emotional stress, feer, trauma, and immunosuppression

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37
Q

When are patients with varicella contagious?

A

1-2 days before the eruption starts until all the lesions have crusted over

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38
Q

How is varicella transmitted?

A

Aerosolized droplets and direct contact with lesional fluid

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39
Q

Pathogenesis of primary to secondary infections in varicella/zoster?

A

The zoster virus goes into the dorsal root ganglion and remains dormant until re-activated, when it replicates and travels own sensory nerves to the skin

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40
Q

Who gets more severe primary infections with varicella?

A

Adults and adolescents

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41
Q

What is the clinical appearance of primary infection with varicella?

A

Cephalocaudal progression of classic “dew-drops on a rose petal” vesicles on an erythematous base that become pustular and then crust

The vesicles will come in crops, so you will see different vesicles at different stages

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42
Q

Can a chicken-pox like clinical presentation occur after varicella vaccine?

A

Yes, usually a much more field

43
Q

What are the symptoms of congenital varicella syndrome?

A

Cutaneous scarring, CNS/ocular/limb anomalies

44
Q

At want point in pregnancy is the fetus at greatest risk for congenital zoster?

A

20 weeks gestation

Can have reactivation zoster infection in childhood

45
Q

What is neonatal varicella?

A

Caused by perinatal exposure to varicella (within 5 days before delivery to 2 days post-delivery) –> leads to severe disease

46
Q

What is the difference between neonatal and congenital varicella?

A

Congenital zoster occurs while the baby is in utero, the worst disease is @ 20 weeks gestation, can get CNS/limb abnormalities.

  • Neonatal occurs between 5 days before delivery until 2 days postdelivery, is a severe manifestation of zoster
47
Q

What is the prodrome sx’s of a zoster outbreak?

A

Itch, tingling, hyperesthesia, and pain. Progresses to painful vesicles in a grouped distribution on an erythematous base

48
Q

What is the most common location for zoster recurrence?

A
  1. Trunk
  2. Face (trigeminal nerve most commonly affected)
  3. Lumbar
  4. Sacral
49
Q

What is postherpetic neuralgia and who is at risk for having it worse?

A

It is persistent pain, potentially chronic after the zoster lesions have resolved. More severe in the elderly.

50
Q

What clinical change can happen in shingles among patients with HIV?

A

Lesions can be more persistent and thickened

51
Q

What is the definition of disseminated zoster?

A

>20 lesions outside the dermatome or in non-adjacent dermatomes. Also affecting 2 or more dermatomes

52
Q

What are some risk factors for disseminated zoster?

A

Immunosuppressed (AIDS, lymphoreticular malignancy, long-term immunosuppressive medication use)

  • These patients are also at risk for life-threatening pneumonitis and or encephalitis
53
Q

What would you be potentially concerned about if you saw zoster lesions on the ear? What complications would you look out for?

A

This could be Ramsay-Hunt syndrome: lesions on the exterior ear. The nerve affected is CN VII so you can get ear pain, vesicles on the tympanic membrane and external auditory canal, ipsilateral facial nerve paralysis, dry mouth/eyes, anterior 2/3 tongue loss of taste, and auditory/equilibrium issues (including tinnitus).

54
Q

What would you be worried about if you saw zoster outbreak on the tip of the nose?

A

Hutchinson’s sign: V1 nasociliary branch is affected and there is a concern for ocular involvement like keratitis, uveitis, acute retinal necrosis and or visual loss.

55
Q

What is the most common ocular form of zoster?

A

Uveitis is most common followed by keratitis

56
Q

Involvement of what nerves by zoster may lead to eye involvement?

A

CN-II, CN-III, CN-V

57
Q

What complications can arise from cervical dermatome involvement of zoster?

A

Motor neuropathy of the arms and diagram weakness

58
Q

Possible complications from zoster involvement in thoracic dermatomes?

A

Abdominal wall pseudohernia and weakness of muscles

59
Q

Possible complications of lumbar dermatome zoster involvement?

A

Motor neuropathy of the leg

60
Q

What complications are possible with sacral dermatome zoster involvement?

A

Urinary hesitancy/retention, also possible dilation, constipation, pseudo-obstruction, reduced anal sphincter tone (also with thoracic/lumbar/sacral zoster)

61
Q

How much an increase in IgG is needed to retrospectively confirm zoster diagnosis?

A

A 4-fold increase in IgG titers can confirm prior infection

62
Q

Most sensitive test for zoster infection?

A

PCR, viral culture is specific but not sensitive. Tzanck smears and DFA are other options.

63
Q

What does zoster need to be treated to be effective?

A

Treatment within 3 days of lesion onset leads to decreased severity and duration of dz

64
Q

What treatment options are frontline for zoster?

A

Oral acyclovir or valacyclovir for immunocompetent/non-disseminated dz.

For immunosuppressed patients and disseminated = IV acyclovir

65
Q

When should varicella-zoster immunoglobulin be given?

A

Should be administered within 96 hours of exposure in immunocompromised, pregnant females and neonates.

66
Q

What type of vaccine is the varicella vaccine and what is its schedule?

A

Live attenuated virus vaccine, is given as a 2-dose series (first dose at 12-15 months and the booster dose at 4-6 years)

67
Q

Who is the Varicella vaccine contraindicated in?

A

Pregnant patients and immunosuppressed

68
Q

What is the prophylaxis of primary varicella infection?

A

The vaccine can be given 72-120 hrs of exposure in nonimmune, zoster Ig can be given within 96 hrs of exposure in immunocompromised/pregnant females and neonates (can also use IVIG), oral acyclovir can be used within 7-10 days of exposure

69
Q

When should treatment be given for zoster?

A

Within 72 hrs of of start of sx’s

70
Q

Treatment for zoster?

A

Can give acyclovir, valacyclovir, or famciclovir. Prednisone can be given for acute pain but doesn’t affect course or development of postherpetic neuralgia.

71
Q

Why is the treatment of zoster important for patients over 50?

A

Treatment decreases the rate of postherpetic neuralgia in these patients. Valacyclovir and famciclovir preferred over acyclovir

72
Q

Treatments for postherpetic neuralgia?

A

TCA, gabapentin, 8% capsacian patch, pregabalin, opioid analgesics, and lidocaine patch

73
Q

How effective is shingrix in preventing shingles?

A

In patients over 50, it is >90% effective in preventing shingles

74
Q

Contraindications to shingrix?

A

A negative immunity test for varicella (should get varicella), pregnant or breastfeeding, severe infection, recently had zostavax (should wait 8 weeks).

Patients who have had shingles should still get the vaccine

75
Q

What conditions can arise from or be related to the Epstein-Barr virus (HHV-4)?

A

Infectious mononucleosis, oral hairy leukoplakia, hydroa vacciniforme, Gianotti-Crosti (#1 in the US), genital ulcers, and various hematologic disorders/malignancies like Burkitt’s lymphoma, NK/T-cell lymphoma, post-transplant lymphoproliferative disorder, and nasopharyngeal carcinoma.

76
Q

How is EBV (HHV-4) transmitted and what cell does it infect?

A

Transmission via saliva/blood –> infects mucosal epithelial cells and then spreads to the B-cells (virus can lay dormant in B-cells and evade immune detection)

77
Q

How does the EBV evade immune detection in B-cells?

A

Production of EBNA-1 protein and latent membrane protein-2

78
Q

What is a risk factor for getting lymphoproliferative disorders after EBV infection?

A

Decreased cell-mediated immunity appears to be more important than humoral. Allows infected B-cells to continue proliferating

79
Q

What rash can occur in a patient with mononucleosis if they are given what antibiotic?

A

Morbilliform, pruritic hypersensitivity rash can occur in patients given amoxicillin who have mononucleosis

80
Q

What are the clinical findings in mononucleosis?

A

Usually young adults with pharyngitis, fever, cervical lymphadenopathy, splenomegaly (+/- hepatomegaly), lymphocytosis (up to 40% atypical lymphs), nondistinct polymorphous rash in 5-10% of cases that shows a centrifugal spread w/ petechial lesions on the eyelid and hard/soft palate junction

81
Q

What is the most common location for oral hairy leukoplakia?

A

Lateral tongue

82
Q

Risk factors for oral hairy leukoplakia?

A

HIV, smoking

83
Q

Ways to make a diagnosis of EBV infection?

A

Monospot test (nonspecific but confirms the presence of IgM heterophilic antibodies which are often present in EBV infxn and can persist for months after infxn), EBV-specific antibodies, + heterophilic antibody (>1:40), PCR TO EBV DNA

84
Q

What group of patients are at higher risk of having a false negative monospot test? And what test should be done instead?

A

Younger children, EBV specific antibodies are more sensitive in younger children (targets against viral capsid antigen, early antigen, and EBNA)

85
Q

What activity should patients with mono be counseled against?

A

Should avoid contact sports/contact activities where splenic rupture could occur until the splenomegaly resolves

86
Q

How can EBV serologies be interpreted in acute infectious mono, convalescent mono, past infection, and reactivation/chronic infection

A

Acute infection: IgG=+, IgM=+, EA=postive/negative, EBNA= negative

Convalescent mono: IgG=+, the rest are variable

Past infection: IgG=+, IgM=negative, EA=low + or neg, EBNA=+

Reactivation: IgG=++, IgM=+/neg, EA=++, EBNA=+/neg

87
Q

How is cytomegalovirus (HHV-5) transmitted?

A

body fluids, fomites, vertical transmission, transplanted organs, and hematopoietic stem cells

88
Q

Pathophysiology of CMV infections?

A

Infects leukocytes –> dissemination –> organs –>latency

89
Q

What is the clinical presentation for most patients and what patients are at risk for serious manifestations?

A

Most patients are asymptomatic (can have a mono-like syndrome), but it can be severe in immunosuppressed (meningoencephalitis, pneumonitis, GI ulcers, eye dz or in-utero (blueberry muffin baby, microcephaly, deafness (most common cause in US), etc)

90
Q

If a beta-lactam is given in a patient with CMV-induced mono, will they get the hypersensitivity rash-like in EBV-caused mono?

A

Yes

91
Q

What complications may be seen from CMV in patients with HIV?

A

Can get recalcitrant ulcers in the perineum or leg, can also get verrucous plaques, vesicles and or nodules

92
Q

What is the pathognomonic finding on histology in ulcers caused by CMV?

A

“Owls eye” intranuclear inclusions in enlarged endothelial cells (cowdry bodies)

93
Q

What are the treatments for CMV related disease?

A

Ganciclovir (IV) and Valganciclovir (oral) are first line

94
Q

What age group is most often affected by Roseola infantum (HHV-6)?

A

95% of patients are between 6 months and 3 years of age.

95
Q

What is one complication that can arise from roseola infantum?

A

In ~15% of infants, they can get febrile seizures

96
Q

Where does the HHV-6 virus remain latent? and what are some conditions associated with reactivation?

A

Lays dormant in T-cells for life. Can lead to DRESS (along with EBV, HHV-7, and CMV), chronic fatigue and pityriasis rosea

97
Q

What diseases has HHV-7 been associated with?

A

It is not definitively causative of anything, but is similar to HHV-6 and has been associated with DRESS, pityriasis rosea, and exanthem subitum (roseola) [somewhat unique presentation when both HHV-6/7 are present]

98
Q

What diseases is HHV-8 associated with?

A

Kaposi sarcoma, multicentric castleman disease, primary effusion lymphoma, and paraneoplastic pemphigus

99
Q

What time of year is roseola infantum (HHV-6) most common?

A

Spring

100
Q

What are the two variants of HHV-6 seen that cause disease and who do they affect?

A

HHV-6A= Seen in HIV + pts

HHV-6B=erythema subitum

101
Q

How is HHV-6/exanthem subitum transmitted?

A

Oral secretions

102
Q

What is the clinical manifestation of exanthem subitum?

A

Incubation period up to 1-2 weeks, high fever (>40*C) for up to 5 days (can have other URI sx’s), then fever remits and exanthem begins.

  • Exanthem: generalized but subtle maculpapular eruption that is predominantly found on the trunk and goes away in 2-3 days
103
Q

What are the red macules seen on the soft palate and uvula in HHV-6/exanthem subitum/roseola called?

A

Nagyama’s spots

104
Q

What is the prognosis for patients with HHV-6 induced exanthem subitum who get seizures? Overall?

A

Benign course. Even true in pregnant women and patients who get febrile seizures (unlikely to have future seizures)

DERM (11) Infections, Infestations, and Bites (13 decks)

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