Herpes zoster is commonly known as shingles. It is a viral disease caused by reactivation of varicella-zoster virus which remains dormant in the sensory ganglia of the cranial nerve or the dorsal root ganglia after a previous varicella infection. Varicella is commonly called as chicken pox occurs in children while herpes zoster occurs in adults or the elderly.
Upon reactivation, the virus replicates in neuronal cell bodies, and virions shed from the cells which are carried down the nerve to the area of skin innervated by that ganglion. In the skin, the virus causes local inflammation and blistering. The pain caused by zoster is due to inflammation of affected nerves with the virus.
The incidence of herpes zoster ranges from 1.2 to 3.4 per 1000 persons per year among younger healthy individuals while incidence is 3.9 to 11.8 per 1000 persons per year among patients older than 65 years. There is no seasonal variation seen with herpes zoster.
Cutaneous lesions of herpes zoster produce Varicella-zoster virus-specific T-cell proliferation, while production of interferonra leads to resolution of herpes zoster. In immunocompetent patients, specific antibodies (IgG, IgM, and IgA) appear more rapidly and reach higher titers during reactivation (herpes zoster) than during the primary infection causing long-lasting, enhanced, cell-mediated immunity to the varicella-zoster virus.
Zoster characteristically presents with a prodrome of fever, malaise, and excruciating burning pain followed by the outbreak of vesicles which appear in one to three crops over three to five days. Lesions are distributed unilaterally within a single dermatome.
Clinically, lesions start as closely grouped erythematous papules which, rapidly become vesicles on an erythematous and edematous base and may occur in continuous or interrupted bands in one, two, or more contiguous dermatomes unilaterally. Dermatomes commonly involved are thoracic (53%), cervical (20%), and trigeminal (15%) including ophthalmic and lumbosacral (11%).
Shingles oticus is also known as Ramsay Hunt syndrome type II. It is due to spreading of the virus from the facial nerve to the vestibulocochlear nerve which involves the ear and causes hearing loss and vertigo (rotational dizziness).
Zoster may occur in the mouth if the maxillary or mandibular division of the trigeminal nerve is affected. Clinically, it presents with vesicles or erosions occurring over mucous membrane of the upper jaw (palate, gums of the upper teeth) or the lower jaw (tongue or gums of the lower teeth). Oral involvement may occur alone or in combination with the lesions on the skin over the cutaneous distribution of the same trigeminal branch.
Due to the close relationship of blood vessels to nerves, the virus can spread to involve the blood vessels compromising the blood supply, and causing ischemic necrosis. Complications such as osteonecrosis, tooth loss, periodontitis, pulp calcification, pulp necrosis, periapical lesions, and tooth developmental anomalies can occur due to it.
The ophthalmic division of the trigeminal nerve is the most commonly involved branch which causes ophthalmic zoster. The skin of the forehead, upper eyelid, and orbit of the eye may be involved. It is seen in approximately 10% to 25% of cases presenting with features of, keratitis, uveitis, and optic nerve palsies. Complications in the form of chronic ocular inflammation, loss of vision, and debilitating pain can occur.
Complications of herpes zoster include secondary bacterial infection, post-herpetic neuralgia, scarring, nerve palsy, and encephalitis in the case with disseminated zoster.
During pregnancy, varicella may lead to infection in the fetus and complications in the newborn, but chronic infection or reactivation, in other words, herpes zoster, is not associated with fetal infection.
Zoster sine herpete is an entity with a pain in the involved dermatome without any skin lesions.
Herpes zoster is clinically diagnosed with burning pain, characteristic morphology, and typical distribution. Herpes simplex virus can occasionally produce a rash in a pattern called as zosteriform herpes simplex.
Tests for varicella-zoster virus include the following:
Molecular biology tests based on in vitro nucleic acid amplification (PCR tests) are currently considered the most reliable. Nested PCR test has high sensitivity, but is susceptible to contamination leading to false-positive results. The latest real-time PCR tests are rapid, easy to perform, as sensitive as nested PCR, have a lower risk of contamination, and also have more sensitivity than viral cultures.
Cutaneous lesions of herpes zoster need to be differentiated from herpes simplex, dermatitis herpetiformis, impetigo, contact dermatitis, candidiasis, drug reactions, and insect bites. Preceding pain without the development of skin lesions in herpes zoster is different from cholecystitis and biliary colic, renal colic, trigeminal neuralgia, or any dental infection.
Herpes zoster tends to involve only one side of the oral cavity, which distinguishes it from other oral blistering conditions. In the mouth, it presents initially as vesicles which break down quickly to leave ulcers that heal within 10 to 14 days. The prodromal pain before the rash may be confused with a toothache which leads to unnecessary dental treatment.
Antiviral therapy hastens the resolution of lesions, decreases acute pain and helps to prevent post-herpetic neuralgia especially in elderly patients. Acyclovir 800 mg, five times daily for five days, valacyclovir 1 gm three times daily for five days, and famciclovir 500 mg three times daily for seven days are the antiviral drugs used to treat herpes zoster. Topical antibiotic creams like mupirocin or soframycin help to prevent secondary bacterial infection. Analgesics help to relieve the pain. Occasionally, severe pain may require an opioid medication. Topical lidocaine and nerve blocks may also reduce pain.
Post-herpetic neuralgia commonly occurs in elderly patients, and once the lesions have crusted, they can use topical capsaicin and Emla cream.