STIs 2 Flashcards
ddx for genital ulcer disease
1. Herpes Simplex Virus (type 2 > type 1)
2. Syphilis (Treponema pallidum)
3. Chancroid (Haemophilus ducreyi)
4. Lymphogranuloma venerium (LGV), caused by C. trachomatis
Herpesviridae - species
- Human virus:
-HSV1 (human herpesvirus 1)
-HSV2 (human herpesvirus 2)
-Varicella zoster virus (HHV-3)
-Epstein Barr virus (HHV-4)
-CMV (HHV-5)
-HHV6
-HHV7
-HHV8 (Kaposi’s sarcoma herpesvirus) - Simian virus:
-Herpes B virus
human herpesviruses - overview
*establish latent infection in specific target cells
*infection persists despite the host immune response, often with recurrent disease
*HSV1, HSV2, VZV, EBV, CMV, etc
herpes simplex virus (HSV) - epidemiology
*most common cause of genital ulcer disease worldwide
*genital herpes most often due to HSV2, but HSV1 becoming more common
*most cases are asymptomatic
*risk related to lifetime number of sex partners, age of sexual debut, and history of other STIs
HSV - transmission
*close contact with person shedding virus:
-inoculation of HSV2 on susceptible mucosal surface or crack in skin
-vertical transmission from mother to fetus during pregnancy/birth
*majority of genital herpes infections are transmitted by persons who are unaware they are infected or aysmptomatic
*incubation period = 2 to 12 days
*drying and soap&water readily inactivate HSV; fomite transmission unlikely
HSV pathogenesis
- exposure to virus → viral replication in epidermis →
- infection of sensory/autonomic nerves →
- intra-axonal transport to nerve cell bodies →
- HSV1 (trigeminal), HSV2 (sacral ganglia) →
- latent virus in sensory ganglion, which then reactivates (recurrent infection):
-triggers: trauma, UV light, immunosuppression
HSV1 - latent cell
*latency in trigeminal nerve
HSV2 - latent cell
*latency in sacral ganglia
HSV clinical manifestations: primary episode
*characterized by multiple lesions that are more severe, last longer, and have higher titers of virus than recurrent infections
*typical lesion progression: papules → vesicles → pustules → ulcers → crusts → healed
*often associated with systemic sx including: fever, headache, malaise, myalgia
*cervicitis, urethritis, perianal infection, proctitis
*illness lasts 2-4 weeks
HSV clinical manifestations: recurrent disease
*usually localized to defined mucocutaneous site
*symptoms more mild, duration shorter
*frequency and number of recurrences decreases over time
*prodromal symptoms
*“atypical” syndromes common (fissures)
genital herpes - diagnosis
*patient history and clinical presentation
*laboratory tests:
-virus detection tests (culture, PCR of lesion)
-serology
HSV treatment
ACYCLOVIR
other options: valacyclovir, famciclovir
*generally treat for 7-10 days
*MOA: all phosphorylated by cellular and herpesvirus kinases that inhibit viral DNA synthesis (requires the virus for the treatment to work)
HSV prevention
*antivirals - decrease transmission by 55%
*condoms - decrease transmission by 30%
HSV - treatment approaches of recurrences
- episodic treatment
- suppressive treatment:
-reduces frequency of recurrences
-reduces but does not eliminate subclinical viral shedding
-periodically, reassess need for continued suppressive therapy
HSV2 - complications
*urinary retention
*sacral radiculopathy
*aseptic meningitis
*pneumonia
*hepatitis
*transverse myelitis, autonomic sx, decreased reflexes/motor strength
syphilis - microbiology
*etiologic agent = Treponema pallidum
*corkscrew-shaped, motile microaerophilic bacterium
*cannot be cultured in vitro; cannot be viewed by normal light microscopy