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MID II > Herpes > Flashcards

Herpes Flashcards

1
Q

What is the structure of herpes viruses?

A

ds DNA virus (low mutation rate)

Enveloped (doesn’t survive well in environment)

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2
Q

How is CMV transmitted?

A

person to person/via infected fomites

Intrauterine

Perinatal: present in cervicovag secretions

Postnatal: breast feeding, daycare, saliva, urine

Blood transfusion

Organ transplantation

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3
Q

How does CMV pathogenesis occur?

A

Infects endothelial cells of GU, upper GI, respiratory tract

Then infects leukocytes & spreads to multiple tissues

Can then become symptomatic disease, asymptomatic infection, or latent infection

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4
Q

Where is the latent CMV reservoir?

A

Myelomonocytic stem cells

Monocytes

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5
Q

What determines whether patienst have asymptomatic infection or symptomatic disease by CMV?

A

Usually asmytomatic, except in immunocmopromised patients with impaired T cell immunity

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6
Q

What are the three common manifestations of symptomatic CMV infection?

A

Infectious mononucleosis

Congenital CMV infection

CMV infection in immunocompromised host (solid organ transplantation, bone marrow transplantation, HIV/AIDS)

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7
Q

What are the symptoms of infectious mono caused by CMV?

A

Fever, hepatomegaly, lymphadenopathy, malaise, fatigue, splenomegaly, pharyngitis, rash

Lab findings: atypical lymphocytes, lymphocytosis, mild thrombocytopenia, CMV antibodies, heterophile antibodies

CMV is responsible for about 8% of IM cases; EBV is the other common cause

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8
Q

What are the symptoms of congenital CMV infection?

A

Hepatosplenomegaly, lymphadenopathy, resp distress, blueberry muffin rash, microcephaly, brain damage –> retardation, seizurse, deafness, blindness

Elevated LFT (liver function tests), thrombocytopenia, pneumonitis, CMV in body fluids

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9
Q

What are common manifestations of CMV diseases in immunocompromised host?

A

Fever, hepatitis, retinitis, pneumonitis, immunosuppression, myelosuppression, encephalopathy, colitis, rejection, graft v host disease

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10
Q

What common disease might be associated with CMV infection?

A

Atherosclerosis

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11
Q

How is CMV diagnosed?

A

Serology– IgG and IgM (note that IgM usually indicates a new infection, but in CMV even reactivations lead to an increase in IgM)

Virus isolation, pp65 antigen detection in blood, CMV DNA PCR

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12
Q

What is the treatment for CMV?

Who should get treatment?

A

Ganciclovir

Valganciclovir

Foscarnet

Cidofovir

All are viral DNA polymerase inhibtors

Used to treat immunocompromsed host

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13
Q

How is HSV transmitted?

A

Person to person

Intrauterine = rare

Perinatal

Postnatal: skin/mucous membrane contact/viral shedding in saliva, oro-facial lesions

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14
Q

Which strain is more common in oral cavity? GU tract?

A

HSV-1 in oral cavity

HSV-2 in GU tract

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15
Q

What are the 3 types of infections that HSV can cause?

A

Primary infection: virus replicates in skin & mucous membranes –> enters nerve endings –> retrograde transport to sensory ganglia –> replication here –> anterograde transport back to mucosal and cutanous sites –> can be released from lesions/ continue to replicate here

Latent infection: reversible interruption of the virus replication cycle in sensory neurons

Reactivation of latent infection: probably due to changes in host; leads to recurrent infections

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16
Q

Why are herpes lesions painful?

A

Bc they replicate in sensory neurons– causes pain!

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17
Q

What are common clinical illnesses caused by HSV infection?

Less common?

A

HSV 1:

  • *gingivostomatitis** (fever, oral pain, difficulty swallowing, vesicular lesions throughout oral cavity)
  • *pharyngitis** (fever, looks like strep, EBV)
  • *labialis** (cold sores)

HSV 1 or 2:

  • *herpes genitalis** (painful genital ulcers)
  • *neonatal herpes** (vesiculoulcerative lesions on skin, eyes mouth, encephalitis, or disseminated infection)

Less common: encephalitis, keratitis, retinitis, gladiatorim (wrestler’s herpes), herpes whitlow (finger), eczema, disseminated herpes, erythema multiforme, bells palsy,

Possibly schizophrenia, alzheimer’s

18
Q

How is HSV infection diagnosed?

A

IgG, IgM

Virus isolation

Antigen detection

DNA PCR

Clinical diagnoses= unreliable

19
Q

How do you treat HSV?

A

Oral acyclovir, valacycolvir (its prodrug), or famciclovir (penciclovir prodrug)

Topical acyclovir/penciclovir

IV Acyclovir

** these drugs are very safe. all are viral DNA pol inhibitors

20
Q

How can you prevent herpes infection- neonatal? Genital?

A

Neonatal: C-section

Genital: condoms, valacyclovir by infected partner

21
Q

What are the 3 categories of herpes infections? Features? Examples?

A

Alpha: short replication cycle, variable host range, latent in sensory neurones
HSV1, 2, VZV

Beta: long reproductive cycle, narrow host range, latent in lymphoid cells & others
CMV, HSV6, HSV7

Gamma: narrow host range, latent in lymphoid cells, associated with tumors
EBV, HSV8= KSH

22
Q

What diseases does VSV cause?

A

Varicella= chicken pox

Zoster = shingles

23
Q

What type of rash is VSV?

A

Vesicular

Highly infectious

24
Q

How does VSV spread in cells?

A

Cell to cell OR from free enveloped particle

This is important bc it can remain intracellular and still spread – antibodies can’t reach it, making cellular immunity critical for host defense against these viruses

25
Q

What is the structure of herpes viruses?

A

Enveloped

Icosahedral capsid

DNA genome- ds

26
Q

Where does VSV get its final envelope in the cell?

A

The transgolgi network

27
Q

What is varicella?

A

Chicken pox- vesicular rash, sheds contagious virus particles which can infect another person via airbourne route

28
Q

What is zoster?

A

Shingles - reactivation of VSV after its been latent post- varicella infection

Presents as vesicular rash, dermatomal distribution, doesn’t cross the midline. Rash is infectious

Happens in the elderly or immunocompromised

29
Q

When can VSV be dangerous i.e. which people?

A

Congenital infection– when mom gets it during pregnancy; affects many organ systems, baby often dies

In immunocompromised: more severe illness, can be fatal

30
Q

What happens to make VSV latent?

A

Stays in the dorsal root ganglia

Expresses only a few genes

Not “lytic”

31
Q

How can you diagnose VSV?

A

immunofluorescence on a smear of the vesicular fluid

PCR of vesicular fluid

Culture

32
Q

How can you prevent VSV?

A

Vaccine: live attenuated vaccine

It’s the only herpes virus for which there is a vaccine

33
Q

How can you treat VSV? Who should get treatment?

A

Acyclovir– requires higher does than for HSV; not that it works best for HSV-1>HSV-2>VSV

SE include Gi symptoms, neuro symptoms, bone marrow suppression

34
Q

What cancer is associated with EBV?

A

Burkitt’s lymphoma

Think: EBV infects B cells and causes Burkitt’s

35
Q

What disease is caused by EBV?

Symptoms?

Treatment?

A

Infects B cells and causes infectious mononucleosis, nasopharyngeal carcinoma, lymphoma (including Burkitt’s), oral hairy leukoplakia, post-transplant lympho-proliferative disease

Latency develops in memory B cells after mono

36
Q

What are the symptoms of infectious mono?

A

Fever, lymphadenopathy, hepatosplenomegaly, exudative pharyngitis, fatigue, rash after treatment with ampicillin

37
Q

How do you diagnose infectious mono?

A

Serology

38
Q

What is roseola?

A

Acute illness in infants - rash, fever, seizures; latent in CNS

39
Q

What is herpes virus 8?

A

Closely related to EBV - gamma virus

Causes Kaposi’s sarcoma in the elderly/HIV infected

40
Q

Which herpes infections cause congenital illness?

Neonatal?

A

Congenital = CMV, VSV

Neonatal = HSV, VSV

** VSV can do both

MID II (22 decks)

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