Flashcards in HSVInfections Deck (33):
Initial HSV Genital Infection:
Had been exposed to HSV somewhere OUTSIDE of genital tract originally (cold sore > genital)
Primary HSV Genital Infection:
First contact with HSV (more severe response)
**Symptoms of HSV Genital Infection (Primary + Initial):
Progress from macules > papules > vesicles > pustules > ulcer **(PAINFUL)**, fever, lymphadenopathy
Recurrent Genital Lesions with HSV:
Will have less lesions (3-5) with a prodrome of tingling and pain.
Infection of digits leading to an ulcer (commonly seen in fingers of healthcare field workers) Caused by HSV infection
Cold Sore - caused by HSV
Herpes Simplex Keratitis:
Initial outbreak: conjunctivitis. Recurrent outbreak can build scar tissue > blindness.
Highest risk for Neonatal Herpes Infection:
When mother has a primary infection at the time of delivery.
Most Neonatal Herpes Infections acquired when?
At birth. HSV not thought to be able to cause infection PRIOR to birth.
Least severe presentation of Neonatal Herpes Infection and its possible complication:
Disease localized to skin, eyes and mouth. Have recurrences in first 6 months and UNTREATED can lead to encephalitis.
Symptoms of Neonatal Herpes Infection: Encephalitis:
This can present WITH or WITHOUT skin lesions. Seizures, lethargy, tremors, bulging fontanel.
Most severe form of Neonatal Herpes Infection:
Disseminated Infection. Will have presence of lesions in wherever it has disseminated to.
Treatment for Neonatal Herpes Infection:
IV administration of antivirals.
HSV Virus Family:
**Genome (?) + Envelope (?) of HSV:
HSV Genome Replication:
Encodes for many of its own enzymes for genome replication. HSV polymerase= target for antivirals.
Life Cycle of HSV Infection:
Attacks epithelium where it can replicate > retrograde transport of HSV in SENSORY NEURON > nucleus > latent infection established.
Life Cycle of HSV Spontaneous Reactivation:
HSV reactivates (due to stress,UV light, trauma, hormones) > anterograde to epithelium > virus replication and shedding in epithelial tissue
HSV-1 Commonly associated with:
HSV-2 commonly associated with:
Over what % of adults are seropositive for HSV-1 or HSV-2?
Primary infection by HSV-1 usually occurs before:
**Diagnosis of HSV:
clinical appearance of lesions: **1-2mm diameter in groups**, Tzanck Smear (cells fused > large multinucleated cell)
Tzanck Smear Appearance and Use:
used for HSV-1 or 2 and Varicella diagnosis
**Differentiating Diagnostically between HSV-1 and 2:
PCR to detect genome or Immunocytochemistry to detect Antigens
What is the treatment of HSV dependent on?
What TYPE of lesions are present.
Treatment of HSV: Oral Lesions:
Generally not treated.
Treatment of HSV: Genital Herpes- Primary and Recurrent:
Primary: oral antivirals Recurrent: long term oral antivirals
Goals of Anti-herpetic Drugs:
To shorten time to lesion healing and increase time between outbreaks
Anti-herpetic drugs do not target what stage:
THEY DO NOT ACT ON LATENT STAGE INFECTION
HSV Antivirals: Nucleoside Analogues MOA:
Viral Thymidine Kinase MUST phosphorylate the drug into monophosphate form= CRITICAL FOR DRUG TO BE ACTIVE. Drug continues to be phosphorylated and looks like nucleotide > chain termination + binds to DNA polymerase. ONLY ACTIVE WITHIN INFECTED CELLS BECAUSE OF NECESSITY FOR VIRAL THYMIDINE KINASE.
**Three types of Nucleoside Analogues for HSV treatment:
Famciclovir, Valacyclovir (ideal for ORAL administration) Acyclovir