HSV/HPV Flashcards
Herpes Simplex Virus: Genital Herpes (Characteristics)
- Lesion progression from macules, papules, vesicles, pustules, to ulcers
- Often fever, inguinal adenopathy, malaise
- Lesion duration is ~3 weeks
- Symptoms more severe in WOMEN
- Common lesion sites: vulva, cervix, peritoneum, penis, thighs, buttocks
PRIMARY infection will be MORE SEVERE; i.e. first time patient has seen the infection
Herpes Simplex Virus: Genital Herpes (Recurrent Lesions)
3-5 Discreet lesions
Vulvar irritation
Prodrome –> Tingling and Pain
Heal within 7-10 days
Herpes Simplex Virus: Other Diseases
1) Herpetic Whitlow (Ulcer on finger; most commoly seen in healthcare field)
2) Herpes labialis (cold sore)
3) Herpes simplex keratitis
4) Herpes simplex encephalitis (Rare but most serious outcome)
Neonatal Herpes Infection
Highest risk is infants born to mothers experiencing PRIMARY infection at time of delivery
Rarely asymptomatic and often lethal
Neonatal Herpes Infection (Localized to Skin, Eyes, and Mouth)
- Not lethal (Least severe, even without treatment)
- Present at 10-11 days following birth
- Recurrences in first 6 months
- ~30% untrated have more serious consequences: BLINDNESS, MICROCEPHALY, SPASTIC QUADRIPLEGIA
Neonatal Herpes Infection (Encephalitis)
May or may not have skin lesions with this
1/3 of nenoate infections
Neurologic symptoms (bulging fontanel, temp instability, poor feeding)
Can be improved with anti-herpes agents
Neonatal Herpes Infection (Disseminated Infection)
Lesions in visceral organs and skin
Symptoms: irritability, seizures, respiratory distress, jaundice, bleeding diathesis, shock
Complications: HSV pneumonitis, Disseminated Intravascular Coagulation (DIC)
Neonatal Herpes Infection (Prevention and Treatment)
Prevention:
Physical exam for lesions
C. section
Healthcare workers: Herpetic whitlow (do not work during active lesion); Orolabial lesions (wear mask while working)
Treatment:
IV administration of antivirals for all neonate herpes cases
Herpes Simplex Virus (Virology)
Herpesvirus family member
Enveloped
dsDNA genome
***Encodes many of its own enzymes for genome replication
-HSV POLYMERASE is a target of ANTI-VIRALS
Herpes Simplex Virus (Infection and Spontaneous Reactivation)
Infection: HSV attack –> Virus replication in peripheral epithelial tissue –> Retrograde transport –> Latency established in ganglia
Spontaneous Reinfection (due to UV light, trauma, hormones): Virions produced –> Anterograde transport to epithelium –> Virus replication in peripheral epithelial tissues –> HSV shedding –> Recurrent lesions
Herpes Simplex Virus (Clinical)
HSV-1 = Oral lesions HSV-2 = Genital lesions
90% of adults are seropositive for HSV-1 or HSV-2
Primary infection:
HSV-1 before age 4 (via contact with lesions or saliva)
HSV-2 sexual activity
Herpes Simplex Virus (Diagnosis)
Clinical appearance of lesions
1-2 mm diameter groups, vesicles –> pustules –> ulcers
TZANCK SMEAR = cells scraped from border of lesion, staining is used to look for CYTOPATHIC EFFECT and LARGE MULTINUCLEATED CELLS (syncytia formation)
Virological Tests (can distinguish between HSV-1 and HSV-2):
- PCR to detect genome
- Immunochemistry to detect antigens
Herpes Simplex Virus (Treatment Goals)
Anti-herpetic drugs DO NOT act on the latent stage of infection
Goal: SHORTERN time to lesion healing and INCREASE time between outbreaks
Herpes Simplex Virus (Treatment Drugs)
Acyclovir, Famciclovir, and Valacyclovir
Inhibit Viral DNA polymerase
MUST be activated by VIRAL THYMIDINE KINASE
Herpes Simplex Virus (Foscarnet)
Nonnucleoside inhibitor
- No HSV tk phosphorylation needed
- Used in cases of ACYCLOVIR-RESISTANT HSV infections
Common in someone who is immune suppressed and under long-time anti-herpetic treatment