The varicella zoster virus (VZV) is part of the herpes group of viruses; its genetic composition and clinical behavior are very similar to those of the herpes simplex virus. The virus enters the body through aspiration of infected droplets, mostly of saliva from previously infected individuals. Varicella is the primary infection produced by VZV and generally affects children. Varicella manifests clinically after a period of incubation of around 2 weeks. The classical skin lesions are vesicles and bullae scattered throughout the body. There is increased body temperature as well as marked pruritus and pain associated with the vesicles. Intraoral vesicles can also be seen especially at the earlier stages of the infection. The oral vesicles do not exceed 3 or 4 in number and soon rupture leaving ulcers. When the primary infection subsides the virus lodges itself in the dorsal ganglia where it remains latent for life. The recurrent infection with VZV, herpes zoster (HZ), is generally seen in adults, specially the elderly or immunocompromised patients. HZ affects 10 to 20% of the population, generally as a single episode. Around 15 to 20% of the total number of cases affect the trigeminal nerve and of those more than 80% involve the ophthalmic branch. Occasionally some patients have more than one recurrence, especially immunocompromised patients such as those with AIDS. HZ is characterized clinically by linear, opaque-withish vesicles which follow the branches of an affected nerve (dermatome). Patients with HZ generally complain of severe pain and occasional paresthesia to the area prior to the development of the vesicles. The most frequently affected site follows the distribution of one or more than one intercostal nerve.
HZ in the facial area follows the distribution of the branches of the trigeminal nerve. The first branch (ophthalmic) is the most frequently affected branch of the fifth pair. Occasionally the facial nerve can also be affected with vesicles erupting in the external ear canal, this presentation is known as the Ramsey Hunt syndrome.
The oral manifestations will be seen when the maxillary and/or the mandibular branches are involved. Both keratinized and non-keratinized mucosas can be affected. When in the maxilla, it is generally seen on the hard palate with a typical linear distribution of the whitish vesicles. When affecting the mandibular branch it generally manifests in the border of the tongue or the lower lip mucosa.
The intraoral vesicles last only a few hours and they breake leaving areas of painful ulcerations. The vesicles in the skin last up to two or three weeks and they generally tend to coalesce forming large bullae. The skin vesicles may break but the majority will crust and heal without breaking. The pain may persist for up to four or five years after the disappearance of the vesicles and it is known as post herpetic neuralgia.
HZ is an opportunistic infection in patients with underlying immune disorders such as leukemia, lymphomas and AIDS. The most severe cases of HZ in immunocompromised patients are bilateral in distribution. The most frequent presentation in the head and neck areas is in the first branch, producing ophthalmic zoster with severe retinitis. Post herpetic neuralgia is also more marked in these patients and continuous treatment with antiviral and analgesic medications are indicated to prevent recurrences and to alleviate pain.
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Therapeutic protocols
Systemic therapy is indicated in all cases
Intravenous acyclovir is used in HIV positive patients with advanced and/or disseminated HZ. Some authors recommend topical capsaicin or tricyclic antidepressant to alleviate the pain associated with postherpetic neuralgia. Intralesional corticosteroid injections can also be used to block nerve conduction in severe cases of postherpetic neuralgia.