Herpes Zoster

Original Editors - Heather Lindsey and Kaycee Stone from Bellarmine University's Pathophysiology of Complex Patient Problems project.

Top Contributors - Kaycee Stone, Heather Dixon, Lucinda hampton, Donald John Auson, Kim Jackson, Elaine Lonnemann, Wendy Walker, Evan Thomas, WikiSysop, Chelsea Mclene and Nupur Smit Shah

Introduction

Herpes Zoster, commonly called shingles, is characterized by a painful rash with blisters. It results from reactivation of the dormant varicella-zoster virus, also known as chickenpox, that reactivates within sensory ganglia. 

Image 1: Shingles rash caused by herpes zoster virus.

The painful rash is associated with an involved nerve root and its associated cranial or spinal nerve dermatome that occurs 3-5 days after transmission of the virus. It will usually only be present on one side of the body because it typically will not cross the midline. However, it can affect both sides of the body at different dermatome levels.

It is believed that zoster occurs due to the failure of the immune defense system to control the latent replication of the virus. The incidence of herpes zoster is strongly correlated to the immune status. Individuals who maintain a high level of immunity rarely develop shingles. The infection is not benign and can present in many ways. Even after herpes zoster resolves, many patients continue to suffer from moderate to severe pain known as postherpetic neuralgia.

Etiology

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.Triggers for herpes zoster include: Emotional stress; Use of medications (immunosuppressants); Acute or chronic illness; Exposure to the virus; Presence of a malignancy. 

• It is acquired from direct contact with infected airborne droplets or with vesicular fluid.

Image 2: Progression of shingles. A cluster of small bumps (1) turns into blisters (2) that resemble chickenpox lesions. The blisters fill with pus, break open (3), crust over (4), and finally disappear. This process takes four to five weeks. A painful condition called post-herpetic neuralgia can sometimes occur. This condition is thought to be caused by damage to the nerves (5), and can last from weeks to years after the rash disappears.

Epidemiology

The incidence of herpes zoster ranges from

• 1.2 to 3.4 per 1000 persons per year among younger healthy individuals
• 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.Recurrences are most common in patients who are immunosuppressed.

Characteristics/Clinical Presentation

Zoster characteristically presents with a prodrome of fever, malaise, and excruciating burning pain followed by the outbreak of vesicles that 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%).

The three phases of the infection include:

• Preeruptive stage presents with abnormal skin sensations or pain within the dermatome affected. this phase appears at least 48 hours prior to any obvious lesions. At the same time, the individual may experience headaches, general malaise, and photophobia.
• The acute eruptive phase is marked by the vesicles and the symptoms seen in the pre-eruptive phase. The lesions initially start as macules and quickly transform into painful vesicles. The vesicles often rupture, ulcerate and eventually crust over. Patients are most infectious in this stage until the lesion dry out. Pain is severe during this phase and often unresponsive to traditional pain medications. The phase may last 2-4 weeks but the pain may continue.
• Chronic infection is characterized by recurrent pain that lasts more than 4 weeks. Besides the pain, patients experience paresthesias, shock-like sensations, and dysesthesias. The pain is disabling and may last 12 months or longer.

The involvement of the CNS is not uncommon. since the virus resides in the sensory root ganglia, it can affect any part of the brain causing cranial nerve palsies, muscular weakness, diaphragmatic paralysis, neurogenic bladder, Guillain Barre syndrome, and myelitis. In severe cases, patients may develop encephalitis.

Image 3: Herpes Zoster Rash

Complications

Complications of herpes zoster include secondary bacterial infection, post-herpetic neuralgia, scarring, nerve palsy, and encephalitis in the case with disseminated zoster.

1. Disseminated zoster is defined as more than twenty skin lesions developing outside the primarily affected area or dermatomes directly adjacent to it. Besides the skin, other organs may also be affected, causing hepatitis or encephalitis making this condition potentially lethal.
2. Post-herpetic neuralgia is the persistence of pain after a month of onset of herpes zoster. It is the commonest side effect seen in elderly patients with involvement of the ophthalmic division of trigeminal nerve.
3. Complications like cranial neuropathies, polyneuritis, myelitis, aseptic meningitis, or partial facial paralysis occur due to the involvement of the nervous system.

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.

Risk Factors

Immunocompromised people, eg people undergoing treatment for cancer, leukaemia, lymphoma, HIV, and patients on immunosuppressive drugs are at an increased risk of developing shingles. Others who are at a higher risk include patients who have had a transplant, have never had the chickenpox virus, or are under a lot of stress. There have been two different age groups that have been identified as having a higher incidence of acquiring shingles. These two groups are college-aged young adults and adults over 70 years old.

Other Risk Factors include:

• Gender (Females > Male)
• Race/Ethnicity (Blacks > White)
• Family history
• Autoimmune Diseases (rheumatoid arthritis, SLE)

Differential Diagnosis

Herpes simplex virus may mimic herpes zoster if it is recurrent and occurring in a dermatomal pattern. Laboratory tests are needed to avoid the misdiagnosis Lymphangioma circumscriptum can also mimic the rash associated with shingles.

Diagnosis

The diagnosis is generally made based upon an examination of the skin and taking a medical history. A skin sample may be taken to determine if the skin is infected by the varicella-zoster virus. Health care providers may run blood tests, which will not diagnose Herpes Zoster but will show elevated white blood cells and antibodies to the virus that causes chickenpox.

Systemic Involvement

Systemic involvement is not generally noted except in patients that are already immunocompromised due to autoimmune disease or taking medication or treatments that decrease immune function.

• A study by Che et al. found that patients with rheumatoid arthritis who were receiving anti-tumor necrosis factor therapy, or TNF blockers, were at a higher risk for developing herpes zoster up to 61%, including severe infections. 
• In the HIV population, herpes zoster occurs at a higher incidence rate, especially complicated herpes zoster with systemic involvement and a rash affecting multiple dermatomes, although this has decreased from previous incidence rates due to anti-retroviral therapy.
• Patients diagnosed with systemic lupus erythematosus and herpes zoster have been documented to have visceral involvement, which included meningeal spread and pancreatitis in a study by Isgro et al.

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.

Physical Therapy Management

TENS

May be used to treat acute pain and reduce the healing time of the rash associated with herpes zoster. It can be used safely with antiretroviral treatment or as the only treatment.

• A recent study in 2012 found that TENS may be at least as effective as traditional pharmacological therapies, and it may help reduce or prevent the risk of developing postherpetic neuralgia.
• TENS therapy generally involves placing two electrodes on the dermatome affected by herpes zoster for 30 minutes five times per weeks for a period of time up to three weeks. Suggested electrical output was 1-5 mA with frequencies ranging from 20 to 40 Hz.

If the facial nerve is affected by herpes zoster and peripheral facial palsy results, facial exercises have been found to be effective. These exercises include exercises to stimulate functional movement in the face, achieve symmetry, to improve motor control, reduce synkinesis, improve perception of movement, and promote emotional expression. Mirror therapy, mime therapy, facial muscular re-education, and Kabat's exercises were found to be effective means of facial rehabilitation techniques.See Neuromuscular Reeducation in Facial Palsy and facial nerve palsy