The virus enters the bloodstream through the respiratory mucosa to form viremia, and varicella or occult infection occurs, after which the virus can be latent in the posterior root ganglion of the spinal cord or in the sensory ganglion of the cranial nerve for a long time. When the body is stimulated (e.g. trauma, fatigue, malignant tumor or post-illness weakness), the latent virus is activated and replicates along the axon of the sensory nerve to the skin in the area innervated by the nerve, resulting in blistering and inflammation and necrosis of the affected nerve. The disease is usually not recurrent because of the long-lasting immunity after healing. Clinical manifestations Typical manifestations Before the onset of the rash, there may be mild malaise, low-grade fever, poor circulation and other systemic symptoms, and the affected skin may have a burning sensation or neuralgia, with obvious pain sensitivity to touch, lasting 1 to 3 days. The most common sites are the intercostal nerve, cervical nerve, trigeminal nerve and lumbosacral nerve innervation areas. The affected area often first appears as a flushed spot, followed by corn- to soybean-sized papules, which are distributed in clusters and do not fuse, and then rapidly turn into blisters with tense, shiny walls and clarified fluid, surrounded by a red halo, with normal skin between clusters of blisters; the lesions are arranged in a band along a peripheral nerve, mostly on one side of the body, and generally do not exceed the midline. Neuralgia is one of the characteristics of the disease and can occur before the onset of the disease or with the lesions, and is often more intense in older patients. The course of the disease is usually 2 to 3 weeks, and temporary pale erythema or hyperpigmentation remains after the blisters dry up and crusts fall off. Special manifestations (1) Ocular herpes zoster is a viral invasion of the ophthalmic branch of the trigeminal nerve, mostly in the elderly, with severe pain, and may involve the cornea to form ulcerative keratitis. (2) Ear herpes zoster is caused by viral invasion of the facial and auditory nerves, manifesting as herpes of the external auditory canal or tympanic membrane. When the geniculate ganglion is involved and the motor and sensory nerve fibers of the facial nerve are also invaded, a triad of facial palsy, otalgia and herpes in the external ear canal may occur, called Ramsay-Hunt syndrome. (3) Postherpetic neuralgia Herpes zoster is often accompanied by neuralgia, which can occur before, during, and after the lesions have healed, but most often disappears after the lesions have completely resolved or within 1 month; in a few patients, the neuralgia can persist for more than 1 month and is called postherpetic neuralgia. (4) Other atypical herpes zoster is associated with differences in the resistance of the patient’s organism and can manifest as strophic (no lesions but neuralgia), incomplete (only erythema and papules appear without blistering and recede), maculopapular, hemorrhagic, gangrenous, and generalized (involving more than 2 ganglia at the same time and producing lesions in multiple areas contralaterally or ipsilaterally); the virus may occasionally spread through the bloodstream and produce a widespread varicella-like rash and Occasionally, the virus may spread through the bloodstream to produce a widespread varicella-like rash and invade organs such as the lungs and brain. Diagnosis The lesions appear as clusters of blisters on the skin and are distributed in bands along one side of the peripheral nerve. There is marked neuralgia with localized lymph node enlargement. The intervening skin is normal. Differential diagnosis The disease sometimes needs to be differentiated from herpes simplex, which occurs at the junction of skin and mucosa, has an irregular distribution, has small, easily broken blisters, is not painful, is seen in the course of febrile (especially hyperthermic) illnesses, and is often prone to recurrence. Occasionally it is confused with contact dermatitis, but in the latter case there is a history of contact, the rash is not related to the distribution of nerves, and there is self-conscious burning and severe itching without neuralgia. In the prodromal phase of herpes zoster and herpes zoster without rash, neuralgia is easily misdiagnosed as intercostal neuralgia, pleurisy, and acute abdominal conditions such as acute appendicitis, and requires attention. Herpes simplex usually has a history of multiple recurrences at the same site, whereas this does not occur in patients with herpes zoster without significant immunodeficiency. Isolation of the virus from blister fluid or testing for VZV, HSV antigen or DNA is the only reliable method for differential diagnosis. Complications Complicated bacterial infections can have serious consequences if the herpes zoster lesion occurs in a specific area, such as the eye. If a bacterial infection develops secondary to herpes zoster, it can lead to full ophthalmoplegia or even meningitis, with sequelae such as loss of vision, blindness, and facial paralysis. Post-herpetic neuralgia Herpes zoster in the front of the head, the first branch of the trigeminal nerve, can cause hair loss and permanent scarring. Pain can persist for some time after the herpes zoster skin damage has healed. In some elderly patients, the neuralgia can last for months or years and can seriously affect sleep and mood, and the more severe pain and longer duration can lead to mental anxiety and depression. Herpes zoster can occur in the trigeminal nerve segment of the face. There is a nerve fiber in the trigeminal nerve, the ophthalmic nerve fiber, and some of the nerve fibers are distributed in the cornea and conjunctiva of the human eye and the whole eye. The patient may suffer from photophobia, lacrimation, pain in the eyes, resulting in loss of vision, or in severe cases, total uveitis leading to blindness. When the herpes virus infects the motor nerve fibers in the facial nerve, facial palsy can occur. The affected eye cannot close, the affected side has a dull facial expression, the corners of the mouth are skewed to the healthy side, and the patient cannot make blowing movements. Causes inner ear dysfunction Herpes zoster that occurs in the earwalls and ear canals can cause symptoms of inner ear dysfunction. Patients show dizziness, nausea, vomiting, hearing impairment, nystagmus, etc. Viral encephalitis and meningitis occur when the herpes virus invades the central nervous system, i.e., the brain parenchyma and meninges of the body, from the nerve roots at the spinal cord upward, resulting in severe headache, jet-like vomiting, convulsions, twitching of limbs, and life-threatening confusion and coma. When the herpes virus invades visceral nerve fibers from the nerve roots at the spinal cord into the body, it can cause acute gastroenteritis, cystitis, and prostatitis, manifested as abdominal cramps, difficulty urinating, and urinary retention.