STI | Genital Herpes | Clinical Medicine

Overview

Ninja Nerd details the clinical aspects of genital herpes, caused primarily by HSV-2 and HSV-1, focusing on their viral structure (double-stranded DNA), tropism for epithelial cells and neurons, and transmission routes including sexual contact and vertical transmission. The presentation covers the pathogenesis, leading to painful vesicular lesions, lymphadenopathy, and systemic flu-like symptoms, as well as neurological complications like meningitis and encephalitis, and diagnostic approaches using PCR and serology, with treatment focusing on antiviral medications like acyclovir to manage outbreaks and reduce shedding, but not cure the latent infection.

Key takeaways

Genital herpes, primarily caused by HSV-2, establishes latency in sacral ganglia, reactivating to cause recurrent painful vesicular lesions and prodromal symptoms.
Neonatal herpes transmission during vaginal delivery is a critical concern, potentially leading to encephalitis, keratitis, or sepsis, necessitating C-sections for mothers with active lesions.
Antiviral medications like acyclovir, valacyclovir, and famciclovir inhibit viral DNA polymerase, reducing viral shedding and outbreak duration but do not cure the latent infection.
Diagnosis of active lesions relies on PCR (NAAT), while past exposure is identified through serology; Tzanck smears show characteristic multinucleated giant cells but are not definitive.
Suppressive antiviral therapy is indicated for frequent outbreaks (>6/year) or to reduce transmission risk to seronegative partners.
Pregnant individuals with HSV-2 receive suppressive therapy from 36 weeks gestation, and delivery mode is determined by the presence of active lesions or prodrome.

Chapters

0:00 Introduction to Herpes Simplex Virus (HSV)

Herpes simplex virus is a double-stranded DNA, enveloped virus.
Two main types: HSV-1 and HSV-2.
Primarily affects epithelial cells and neurons, including trigeminal and sacral ganglia.

5:45 HSV-1 vs. HSV-2: Location and Ganglia

HSV-1 predominantly affects areas above the waistline (oral/perioral).
HSV-2 predominantly affects areas below the waistline (anogenital).
HSV-1 latency in trigeminal ganglia; HSV-2 latency in sacral ganglia.

11:46 Transmission Routes of Genital Herpes

Primarily transmitted through sexual contact, can be asymptomatic (viral shedding).
Vertical transmission from mother to infant during vaginal delivery is a significant risk.
Asymptomatic shedding can occur even without active lesions.

13:35 Neonatal HSV Complications

Neonatal HSV can lead to encephalitis, keratitis, and disseminated disease/sepsis.
Encephalitis carries a high mortality rate for newborns.
Keratitis can result in blindness.
Sepsis is a life-threatening complication.

16:44 HSV Viral Replication Cycle

HSV binds to epithelial cell receptors and fuses, releasing its DNA.
Viral DNA undergoes transcription (mRNA) and replication (DNA polymerase).
Viral mRNA is translated into capsid and envelope proteins.
New virions are assembled and released from the cell.

23:35 Therapeutic Targets and Diagnostics

Viral DNA polymerase is a key target for antiviral drugs.
Antivirals like acyclovir, valacyclovir, and famciclovir inhibit DNA polymerase.
Diagnosis can involve viral culture (less preferred) or nucleic acid amplification tests (NAATs).

25:37 Pathogenesis: Cell Fusion and Lesion Formation

HSV induces cell membrane fusion, creating multinucleated giant cells.
Lysis of these giant cells leads to the formation of genital lesions.
Multinucleated giant cells with Cowdry type A and B inclusions can be seen on Tzanck smears.

30:53 Clinical Presentation of Primary Genital Herpes

Characterized by painful vesicular lesions that can coalesce into ulcers.
Associated with painful inguinal lymphadenopathy (lymphadenopathy).
May present with a systemic flu-like syndrome (fever, malaise).

40:07 Neurological Complications: Meningitis and Encephalitis

HSV-2 more commonly causes meningitis.
HSV-1 more commonly causes encephalitis.
HSV encephalitis presents with personality changes, seizures, and focal deficits, often with temporal lobe lesions on MRI.

45:19 Neural Spread, Latency, and Reactivation

Virions travel retrogradely via axons to the dorsal root ganglia (sacral for HSV-2, trigeminal for HSV-1).
Virus enters a latent state in the ganglia, becoming dormant.
Reactivation triggered by stressors (sunburn, stress, immunosuppression) leads to anterograde transport down the axon.

50:50 Rare Complications: Sacral Radiculitis and Mollaret's Meningitis

Rarely, HSV can cause sacral radiculitis (Erb's syndrome) affecting bladder, bowel, and sensation (saddle anesthesia).
Mollaret's meningitis is a rare, recurrent, benign form of HSV meningitis.
Anterograde transport causes recurrent ulcers and prodromal symptoms (tingling, burning).

Summary, takeaways, and chapters were generated by AI from the video's transcript and may contain errors. The video belongs to its creator, Ninja Nerd.