## Why Reactivation of latent varicella-zoster virus from the dorsal root ganglion is right Herpes zoster (shingles) is caused by reactivation of latent varicella-zoster virus (VZV, HHV-3) that remains dormant in the dorsal root ganglia or trigeminal ganglion after primary varicella infection. The virus reactivates along a single dermatome, producing the pathognomonic unilateral, dermatomal vesicular eruption with a sharp cut-off at the midline—exactly as seen in the marked distribution **C**. This anatomical correspondence between the affected ganglion and the dermatomal distribution is the defining feature of zoster. (IADVL Textbook 4e / Fitzpatrick 9e) ## Why each distractor is wrong - **Hematogenous dissemination**: While varicella (primary infection) spreads hematogenously, zoster is NOT a disseminated primary infection. It is reactivation of latent virus from a single ganglion, which is why it remains dermatomal and unilateral. Disseminated zoster (>20 lesions outside the primary dermatome) occurs only in immunocompromised patients and is a complication, not the mechanism of typical zoster. - **Ascending lymphatic spread along the thoracic spine**: Lymphatic spread would not produce the sharp midline cut-off or the precise dermatomal boundary. The dermatomal pattern reflects the sensory distribution of a single spinal nerve, not lymphatic drainage pathways. - **Direct inoculation via minor trauma**: This would cause a localized skin infection, not a dermatomal eruption. Zoster is not acquired from external inoculation but from internal reactivation of latent ganglionic virus. **High-Yield:** Zoster = reactivation from dorsal root/trigeminal ganglion → unilateral dermatomal eruption with midline cut-off; varicella = primary infection → disseminated vesicles. [cite: IADVL Textbook 4e / Fitzpatrick 9e]
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