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Clinical Note |

Pharyngolaryngeal Zoster A Case Report

Po-Shao Chen, MD; Yuan-Yung Lin, MD; Bor-Rong Huang, MD
Arch Otolaryngol Head Neck Surg. 2012;138(6):592-595. doi:10.1001/archoto.2012.600.
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Together with herpes simplex virus (HSV), varicella zoster virus (VZV), also called human herpesvirus 3, is a member of the subfamily of Alphaherpesviridinae. Varicella zoster virus causes chickenpox, which becomes latent in the cranial nerve and dorsal root ganglia and can reactivate many years later to produce shingles. The commonest cause of viral recrudescence is decline in cell-mediated immunity.1

Varicella zoster virus infection of the head and neck is characterized by unilateral distribution of herpetic eruptions and neuralgia. Neurologic involvement, leading to paralysis in the head and neck areas, is common, especially in the facial and vestibulocochlear nerves.2 Zoster complicated with pharyngolaryngeal eruptions without skin lesions and without vocal fold paralysis is extremely rare. Herein, we present the case of a 33-year-old man with VZV infection with glossopharyngeal and internal superior laryngeal nerve (ISLN) paralysis. Our institutional review board deemed this report exempt from review because it is not a research study.

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Figure 1. Laryngeal endoscopic images. A, Indirect laryngoscopy shows white spots on the left palatine tonsil and posterior pharyngeal wall. B, The spots are localized on unilateral left arytenoid cartilage, aryepiglottic fold, posterior pharyngeal wall, and pyriform sinus. There is free movement in the vocal folds.

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Figure 2. Amplification products were analyzed by electrophoresis in 6% polyacrylamide gel and detected by staining with ethidium bromide. Lane A, 100–base pair marker; lanes B and C, swab from the area nearby the lesion; lanes D and E, swab from the lesion; lane F, negative control; lane G, positive control. Lanes D and E show the 267–base pair polymerase chain reaction products of the thymidine kinase gene from varicella zoster virus DNA.




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