HIV - Herpes zoster

Herpes zoster, zona or shingles results from reactivation of latent varicella zoster virus. The initial infection with this virus will result in chickenpox. Afterwards, the virus will stay dormant in the dorsal root ganglia and cranial nerve ganglia. The reactivation will result in a totally different clinical picture. There will inflammation of the posterior and anterior horns of the gray matter, the meninges, and the dorsal and ventral roots. This can proceed subclinical. Skin lesions will appear in a dermatome and sometimes in adjacent dermatomes. The initial symptom is often pain along the site of the future eruption. This pain precedes the rash by 2-3 days. Afterwards, characteristic crops of vesicles will appear. These have an erythematous base. Hyperaesthesia of the affected zone might develop. Dissemination to other parts of the skin and/or to visceral organs can occur, especially in immunodepressed people. Although fewer than 4% of non-immunedepressed people will experience a recurrence, new flare-ups are common in AIDS patients. Postherpetic neuralgia can persist for many months, even years. When herpes zoster affects the otic/geniculate ganglion, geniculate zoster, better known as the Ramsay Hunt syndrome will follow. Pain in the ear and facial paralysis will follow. There will be a vesicular eruption in the external auditory canal. Taste may be lost in the anterior two thirds of the tongue. If the gasserian ganglion in affected, ophthalmic herpes zoster will appear. A vesicular rash in the distribution area of this branch of the fifth cranial nerve is typical. Vesicles on the tip of the nose are a warning sign which indicate involvement of the nasociliary nerve. In this case, corneal lesions are to be expected (75% probability). If there is no lesion on the tip of the nose, the eyeball is involved in 30% of patients. Herpetic keratitis is vision-threatening.