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HDID Block 3 > Herpes Viruses 1 + 2 > Flashcards

Herpes Viruses 1 + 2 Flashcards

1
Q

Which viruses in the Herpes family make up the alpha viruses?

Name 2 things these viruses all have in common

A

Alpha viruses: HSV1, HSV2, VSV

All have short replicative cycles, lie dormant in sensory ganglia**

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2
Q

WHich 3 viruses comprise the beta viruses of the Herpes family?

A

Beta viruses: CMV, HHV6 and HHV 7

All have long replicative cycles and lie dormant in secretory glands, kidneys, WBCs etc

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3
Q

Gamma herpes viruses include ___. What are 2 things these viruses have in common?

A

Gamma herpes viruses: EBV, HHV8

Specifically infect T or B cells and lie dormant in lymphoid tissue

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4
Q

2 major clinical diseases caused by VZV are ___

How is VZV transmitted?

A

Chicken Pox (Varicella)

Shingles (Zoster)

Transmission: respiratory

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5
Q

Manifestation of primary VZV infection is ___ and is a disease of childhood. ___ is VZV reactivation that happens predominantly in older folks.

A

Manifestation of primary VZV infection is Chicken Pox and is a disease of childhood. Shingles is VZV reactivation that happens predominantly in older folks

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6
Q

Describe the clinical manifestation of chicken pox

A

Main symptoms of chicken pox are non-specific febrile illness with malaise, pruritis, anorexia followed by a rash (macule >> papule >> vesicle) at varying stages in different parts of the body

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7
Q

Besides the rash, chicken pox can cause multiple complications. Name them. (hint: 2 are CNS and one in the chest)

A

**2 are CNS: Cerebellar ataxia; encephalitis

**in the chest: pneumonitis

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8
Q

Describe the manifestation of VZV reactivation disease

A

VZV reactivation manifests as Shingles (aka what dad had back in 2015)

Presentation: unilateral vesicular lesions following a dermatome pattern (normally thoracic or lumbar); lesions are preceded by pain 2-3 days prior (also hyperesthesia, paresthesia); acute neuritis

(dermatomes maybe make sense b/c this is a thing that hides in the nerves)

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9
Q

A condition that can occur following Herpes Zoster is ___ (hint: its a pain thing)

A

Pst herpetic neuralgia

(basically a constant, really bad pain condition that lasts for months+ following infection)

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10
Q

What is Herpes Zoster Ophthalmicus?

What is one way to tell that this condition is occuring/will occur soon?

A

It’s basically the same herpes zoster reactivation disease except its on the dermatome of the ophthalmic division of trigeminal nerve (so it happens on the face)

Lesion of tip of nose (Hutchinson’s sign)

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11
Q

Which syndrome results from Herpes Zoster and is characterized by reactivation from the 7th cranial nerve ganglion?

The main sysmptoms, which are __, arise from additional involvement of which cranial nerve? (hint: it’s very close to 7)

A

Ramsay Hunt Syndrome:

Seventh cranial nerve (geniculate) ganglion involvment:

weakness or paralysis of ipsilateral facial muscles, rash in the ears (aka zoster oticus), and involvement of CN8 (tinnitus, hearing loss, nausea, vomiting, vertigo, nystagmus)

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12
Q

What is the main way to Dx VZV disease?

A

History and Physical

**if unsure:

antibody evidence for recent infection (IgM +/- IgG) or seroreversion (IgM + IgG) – look for VZV antibodies

Tzanck or Pap smear of skin lesion scraping – remember that this is non specific (coz 3 other herpes viruses can cause this)

Direct fluorescent antibody (DFA) stain of skin lesion scraping

Culture skin lesion fluid - not really because they take forever to grow

PCR of cerebrospinal fluid

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13
Q

What is the Rx for VZV?

A

Want to think about “ovir” drugs

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14
Q

Describe the 2 vaccines for Varicella (specifically, there’s a chicken pox vaccine)

A

Zostavax – live attenuated zoster vaccine

Shingrix - Inactivated recombinant vaccine

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15
Q

Which Herpes virus causes infectious mononucleosis?

How is this virus transmitted? Which immune cells does the virus primarily infect?

A

Epstein Barr Virus (EBV)/HHV4

Transmission:

exposure to oral secretions (kissing, sharing food, etc)

EBV mainly infects B cells (EBV likes B)

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16
Q

How can EBV infection lead to malignancy? (hint: effects on cell cycle)

A

EBV infected B cells enter the cell cycle and are basically programmed to proliferate indefinitely

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17
Q

Describe the monospot test used to detect EBV infection

A

Monospot test for mononucleosis: basically, pts Abs following EBV infection can bind to different mammalian spp (i.e. heterophiles) and aren’t actually active against EBV proteins

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18
Q

Describe the presentation of primary infection with Epstein Barr Virus

A

Mono presentation: triad w/ fever, sore throat, lymphadenopathy

**know that this infection is generally self ltd and will resolve in a few weeks**

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19
Q

Because infectious mononucleosis can often look like other infections such as Strept throat (b/c pts also have an exudate), pts are often precribed ampicillin which results in what kind of reaction?

A

Ampicillin induced rash

20
Q

What are the complications arising from EBV infection? (hint: heme + spleen!)

A

Heme ones: autoimmune hemolytic anemia; thrombocytopenia

Spleen one: risk of splenic rupture from hepatosplenomegaly

(others: neurological - encephalitis, Guillan Barre, etc; hepatic; renal (hematuria, proteinuria, rhabdomyolysis)

21
Q

Besides infectious mononucleosis, EBV can also cause __ (hint: typically seen in HIV infected patients)

A

Oral Hairy Leukoplakia (note that you CANNOT scrape this off - biggest difference between this and Candida (which you can scrape off) )

22
Q

You just need to see this one

A
23
Q

How do you Dx EBV infection?

A

Atypical lymphocytosis (note that this is non-spefici and other things cause this: CMV, HHV-6 (roseola), HIV, Toxo, viral hepatitis, rubella, mumps)

Monospot for heterophile antibodies

EBV Specific Abs

EBV PCR

24
Q

Interpret the graph below

A

Antibodies to viral capsid antigen (VCA) - IgM and IgG- IgM goes away by 3 mths so if present, suggests acute infection. IgG persists so if present, pt has probably had it before

Antibodies to Nuclear Antigen (EBNA) - if IgG present, suggests that this is NOT an acute mono infection

Antibodies to early antigen (EA) - if IgG present, suggests acute infection

25
Q

How can one contract Cytomegalovirus infection?

A

**see below: but basically its mainly contact with any kind of bodily fluid**

26
Q

Since CMV can also cause infectious mononucleosis, how can you test which virus (EBV vs CMV) is causing mono?

How else does CMV primary infection manifest?

A

Presentation is pretty much the same but CMV infectious mononucleosis tests NEGATIVE on the Monospot (so no heterophile antibodies) AND no exudative pharyngitis!!

other manifestation: non-descript febrile illness in young children; predominantly asymptomatic

27
Q

How does CMV mononucleosis present?

A

Mainly malaise (+ fever + sweats so pretty non specific), elevated LFTs and again, NO exudative pharyngitis

**note that complications are basically the same ones that EBV has**

28
Q

T/F: CMV infected mothers aren’t at risk of transmitting the infection to the baby

A

Falsehood. Congenital infection is real (but depends because if mom has antibodies, they will be protective but if there’s an acute infection while pregnant, there’s a high risk of vertical transmission)

29
Q

What is an ocular manifestation of CMV infection?

How is this disease treated?

A

CMV Retinitis

* most common serious ocular complication of AIDS*

Presents with basically any symptom you can think of that suggests eye disease

Rx: again, “ovir” drugs (1st choice = oral valganciclovir; for sight threatening lesions = intravitreal injection or implant + oral Valganciclovir or intravenous ganciclovir)

30
Q

What is the GI manifestation of CMV and how do you Rx/Dx it?

A

CMV GI disease: esophagitis and colitis

Dx: biopsy showing inclusion bodies

Rx: Ganciclovir (another ovir)

31
Q

What is the manifestation of CMV in the lungs?

A

CMV Pneumonitis (pretty uncommon but if you see it, its a marker of a pt being severely immunocompromised)

*To determine if CMV infection is the cause of disease, do a biopsy and the cells show those inclusion body things*

32
Q

How do you Dx CMV infection?

A

Culture (but as always, takes forever) w/ human fibroblasts

Urine sediment showing inclusion bodies
(Owl’s eyes)

+/- PCR

33
Q

How do you treat CMV infection?

What are the major adverse effects of ganciclovir? (hint: systems affected - CNS, GI and heme)

A

Ganciclovir (note that Valganciclovir is an oral drug)

**this drug needs to phosphorylated first by a phosphotransferase to become active**

Advserse events: fever, diarrhea, thrombocytopenia

34
Q

___ is a CMV drug that directly binds DNA polymerase and inhibits it. Can also be used to treat acyclovir-resistant HSV

A

Foscarnet

**Just think of a fox in a car trying to drive through a net?**

**for side effects: your main ones are hematologic - anemia and granulocytopenia** among other effects in various parts of the body

35
Q

___ is a nucleotide cytosine analogue that can also be used to treat Acyclovir resistant HSV

A

Cidofovir (apparently this is also not a good drug b/c it can cause side effects - renal tubular necrosis - so there’s that)

36
Q

__ is a beta herpes virus that causes 6th disease

A

HHV-6 (note that this bug likes to infect white cells)

37
Q

Describe the rash that’s caused by HHV6

A

6th disease aka roseola infantum aka exanthema subitum

Blanching – rash is red but if you push on it, the redness goes away

Note that the patient presents with a high fever then the fever goes away but then they get a rash after – basically similar to how parvovirus 5th disease presents but the difference is 1, ain’t no slapped cheeks first with this one, and 2, the rash is blanching.

Rash starts on neck then spreads to face and extremities

38
Q

___ is a herpes virus that causes Kaposi Sarcoma (remember this is the one that’s ass’d with HIV)

A

HHV8

39
Q

The main concerns for HHV8 are 3 malignancies, namely __

A

Karposi’s sarcoma

Primary effusion lymphoma

Multicentric castleman’s disease

40
Q

Name the types of Kaposi’s sarcoma (4)

A

Classical KS - mostly in older dudes from the Mediterranean

Endemic KS - mostly in young folks in Sub Saharan Africa

Transplant related KS - you either get KS from an infected solid organ donor, or you already an unknown underlying infection with HHV8

Epidemic KS (this is the AIDS related one)

41
Q

Which disease process is shown below?

A

Kaposi’s sarcoma

42
Q

Describe the manifestations of KS

A

There’s the lesions on the skin and mucous membranes, then there’s the KS in the conjunctiva, oral cavity and pulmonary KS (which is fatal sans treatment)

43
Q

What is the treatment of cutaneous vs visceral KS?

A

For cutaneous KS, you give ART. For visceral KS, Rx = chemotherapy

44
Q

How do you Dx KS?

A

pathology: look for spindle cells (elongated cells suggestive of sarcoma)

presence of HHV-8 on staining

HHV-8 PCR

Clinical

45
Q

Also need to just see this one

A

HDID Block 3 (19 decks)

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