Herpes zoster

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; L. Katie Morrison, MD; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]Vishal Devarkonda, M.B.B.S[3]

Herpes zoster (or simply zoster), commonly known as shingles, is a viral disease characterized by a painful skin rash with blisters in a limited area on one side of the body, often in a stripe. The initial infection with varicella zoster virus (VZV) causes the acute (short-lived) illness chickenpox, and generally occurs in children and young people. Once an episode of chickenpox has resolved, the virus is not eliminated from the body but can go on to cause shingles—an illness with very different symptoms—often many years after the initial infection.

Varicella zoster virus can become latent in the nerve cell bodies and less frequently in non-neuronal satellite cells of dorsal root, cranial nerve or autonomic ganglion,^[1] without causing any symptoms.^[2][3] In an immunocompromised individual, perhaps years or decades after a chickenpox infection, the virus may break out of nerve cell bodies and travel down nerve axons to cause viral infection of the skin in the region of the nerve. The virus may spread from one or more ganglia along nerves of an affected segment and infect the corresponding dermatome (an area of skin supplied by one spinal nerve) causing a painful rash.^[4][5] Although the rash usually heals within two to four weeks, some sufferers experience residual nerve pain for months or years, a condition called postherpetic neuralgia. Exactly how the virus remains latent in the body, and subsequently re-activates is not understood.^[1]

Throughout the world the incidence rate of herpes zoster every year ranges from 1.2 to 3.4 cases per 1,000 healthy individuals, increasing to 3.9–11.8 per year per 1,000 individuals among those older than 65 years.^[6][7][8] Antiviral drug treatment can reduce the severity and duration of herpes zoster, if a seven to ten day course of these drugs is started within 72 hours of the appearance of the characteristic rash.^{[6][9] [10] [11] [12] [13][14]}

Herpes zoster has a long recorded history, although historical accounts fail to distinguish the blistering caused by VZV and those caused by smallpox,^[15] ergotism, and erysipelas. It was only in the late eighteenth century that William Heberden established a way to differentiate between herpes zoster and smallpox,^[16] and only in the late nineteenth century that herpes zoster was differentiated from erysipelas. The first indications that chickenpox and herpes zoster were caused by the same virus were noticed at the beginning of the 20th century. Physicians began to report that cases of herpes zoster were often followed by chickenpox in the younger people who lived with the shingles patients. The idea of an association between the two diseases gained strength when it was shown that lymph from a sufferer of herpes zoster could induce chickenpox in young volunteers. This was finally proved by the first isolation of the virus in cell cultures, by the Nobel laureate Thomas H. Weller in 1953.^[17]

The causative agent for herpes zoster is varicella zoster virus (VZV), a double-stranded DNA virus related to the Herpes simplex virus group. Most people are infected with this virus as children, and suffer from an episode of chickenpox. The immune system eventually eliminates the virus from most locations, but it remains dormant (or latent) in the ganglia adjacent to the spinal cord (called the dorsal root ganglion) or the ganglion semilunare (ganglion Gasseri) in the base of the skull.

Shingles can only arise in individuals who have been previously exposed to chickenpox (varicella zoster). After a person recovers from chickenpox, the virus stays in the body in a dormant (inactive) state. Herpes zoster is not caused by the same virus that causes genital herpes, a sexually transmitted disease.The disease arises from various events which depress the immune system, such as aging, severe emotional stress, severe illness, immunosuppression or long-term use of corticosteroids.^[18][19] The cellular and immunological events that lead to reactivation are poorly understood.^[20] There have been recorded cases of outbreaks occurring due to unmanaged stress or other stresses to the skin such as pinching, biting or scratching of more sensitive areas, such as nipples, ears, and underarms.

[[Diagnosis might not be possible in the absence of a rash (i.e., before rash or in cases of zoster without rash). It is sometimes confused with herpes simplex, and, occasionally, with impetigo, contact dermatitis, folliculitis, scabies, insect bites, papular urticaria, candidal infection, dermatitis herpetiformis, and drug eruptions.sis]] of Herpes zoster

Before introduction of varicella vaccine in the United States in 1995, varicella was endemic, with virtually all persons being infected by adulthood. Since implementation of the varicella vaccination program, incidence has declined in all age groups, with the greatest decline among children aged 1-4 years. Data from passive and active surveillance have indicated a decline in varicella cases of 70%-84% from 1995 through 2001 (1-3). The downward trend in varicella has continued in the United States through 2005 with an approximately 90% decline in incidence from 1995 in active surveillance sites with high vaccine coverage(CDC, unpublished data).

Shingels are developed in patients who were previously infected with VZV (through natural infection that caused varicella or varicella vaccination).All older adults in the United States are at risk for herpes zoster as approximately 99.5% of people born in the United States who are 40 years of age and older have had varicella. Common risk factors include increasing age, immunosupression and stress.

There is no recommended screening guideline for herpes zoster.^[21]

The earliest symptoms (constituting the prodrome) of shingles include headache, sensitivity to light, fever, and malaise, all of which may be followed by itching, tingling, and pain within one to seven days.The rash and pain usually subside within 3 to 5 weeks. Many patients develop a painful condition called postherpetic neuralgia, which is often difficult to manage. Postherpetic neuralgia is most common complication of Herpes zoster.

A detailed history must be taken regarding the onset of symptoms, distribution and morphologic features of rash, accompanying symptoms, such as fever and pruritus and history of previous chicken pox infection must be obtained.

The characteristic physical examination finding of herpes zoster is the maculopapular rash. The rash in typically unilateral and its distribution is confined to one or two adjacent dermatomes. As the rash crusts and heals in 7-10 days, a post-inflammatory hyperpigmentation of the skin may result. Other findings, such as cranial and peripheral nerves involvement depend on the location of the dorsal root ganglia involved.

Laboratory testing may be useful in cases with less typical clinical presentations, such as in immunosuppressed persons who may have disseminated Herpes zoster (defined as appearance of lesions outside the primary or adjacent dermatomes).

Herpes zoster infection can simulate chest pain of cardiac origin. These patients have normal electrocardiographic findings. However, in very rare instances, herpes zoster infection can have cardiac complications, such as myocarditis, endocarditis, pericarditis and others.

A chest x-ray may be done to rule out other causes of chest pain.

Imaging is not routinely done to diagnose herpes zoster infection. However, it may be used as part of the work-up of the several but rare complications of herpes zoster infection.

There are no other diagnostic studies for herpes zoster infection.

Several antiviral medicines—acyclovir, valacyclovir, and famciclovir—are available to treat shingles. These medicines will help shorten the length and severity of the illness. But to be effective, they must be started as soon as possible after the rash appears. Thus, people who have or think they might have shingles should call their healthcare provider as soon as possible to discuss treatment options. Analgesics (pain medicine) may help relieve the pain caused by shingles. Wet compresses, calamine lotion, and colloidal oatmeal baths may help relieve some of the itching.

The only way to reduce the risk of developing shingles and the long-term pain that can follow shingles is to get vaccinated. A vaccine for shingles is licensed for persons aged 60 years and older.^[22]

Infection-control measures after exposure to herpes zoster depend on whether the patient with herpes zoster is immunocompetent or immunocompromised and on whether the rash is localized or disseminated. In all cases, standard infection-control precautions should be followed.

A live vaccine for VZV exists, marketed as Zostavax.^[23] A systematic review by the Cochrane Library concluded that Zostavax can reduce the incidence of herpes zoster by almost 50%.^[24] A 2007 study found that the zoster vaccine is likely to be cost-effective in the U.S., projecting an annual savings of $82 to $103 million in healthcare costs with cost-effectiveness ratios ranging from $16,229 to $27,609 per quality-adjusted life year gained.^[25] In October 2007 the vaccine was officially recommended in the U.S. for healthy adults aged 60 and over.^[23][26]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; L. Katie Morrison, MD; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Herpes zoster has a long recorded history, although historical accounts fail to distinguish the blistering caused by VZV and those caused by smallpox, ergotism, and erysipelas. It was only in the late eighteenth century that William Heberden established a way to differentiate between herpes zoster and smallpox, and only in the late nineteenth century that herpes zoster was differentiated from erysipelas. The first indications that chickenpox and herpes zoster were caused by the same virus were noticed at the beginning of the 20th century. Physicians began to report that cases of herpes zoster were often followed by chickenpox in the younger people who lived with the shingles patients. The idea of an association between the two diseases gained strength when it was shown that lymph from a sufferer of herpes zoster could induce chickenpox in young volunteers. This was finally proved by the first isolation of the virus in cell cultures, by the Nobel laureate Thomas H. Weller in 1953.

• Herpes zoster has a long recorded history, although historical accounts fail to distinguish the blistering caused by VZV and those caused by smallpox,^[1] ergotism, and erysipelas.
• In the late eighteenth century, William Heberden established a way to differentiate between herpes zoster and smallpox.^[2]
• In the late nineteenth century that herpes zoster was differentiated from erysipelas.
• The first indications that chickenpox and herpes zoster were caused by the same virus were noticed at the beginning of the 20th century.
• Physicians began to report that cases of herpes zoster were often followed by chickenpox in the younger people who lived with the shingles patients. The idea of an association between the two diseases gained strength when it was shown that lymph from a sufferer of herpes zoster could induce chickenpox in young volunteers.
• In 1953, Thomas H. Weller was the first who proved association between chickenpox and shingles by the first isolation of the virus in cell cultures.^[3]
• Until the 1940s, the disease was considered benign, and that serious complications were thought to be very rare.^[4]
• In 1942, it was recognized that herpes zoster was a more serious disease in adults than in children and that it increased in frequency with advancing age.
• During the 1950s, further investigation was done on immunosuppressed individuals showed that the disease was not as benign as once thought, and the search for various therapeutic and preventive measures began.^[2]
• By the mid-1960s, several studies identified the gradual reduction in cellular immunity in old age, observing that in a cohort of 1,000 people who lived to the age of 85, approximately 500 would have one attack of herpes zoster and 10 would have two attacks.^[5]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; L. Katie Morrison, MD; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]

The causative agent for herpes zoster is varicella zoster virus (VZV), a double-stranded DNA virus related to the Herpes simplex virus group. Most people are infected with this virus as children, and suffer from an episode of chickenpox. The immune system eventually eliminates the virus from most locations, but it remains dormant (or latent) in the ganglia adjacent to the spinal cord (called the dorsal root ganglion) or the ganglion semilunare (ganglion Gasseri) in the base of the skull.

Multiple names are used to refer to same virus, creating some confusion. Varicella virus, zoster virus, human herpes 3 (HHV-3), and Varicella zoster virus (VZV) all refer to the same viral pathogen. The disease caused by this pathogen is called chickenpox or Varicella disease during the initial infection. A reactivation of the infection is commonly called shingles, herpes zoster or simply zoster.

VZV is closely related to the herpes simplex viruses (HSV), sharing much genome homology. The known envelope glycoproteins (gB, gC, gE, gH, gI, gK, gL) correspond with those in HSV, however there is no equivalent of HSV gD. VZV virons are spherical and 150-200 nm in diameter. Their lipid envelope encloses the nucleocapsid of 162 capsomeres arranged in a hexagonal form. Its DNA is a single, linear, double-stranded molecule, 125,000 nt long.

The virus is very susceptible to disinfectants, notably sodium hypochlorite. Within the body it can be treated by a number of drugs and therapeutic agents including aciclovir, zoster-immune globulin (ZIG), and vidarabine.

Even when clinical symptoms of varicella have resolved, VZV remains dormant in the nervous system of the host in the trigeminal and dorsal root ganglia. In about 10-20% of cases, VZV reactivates later in life producing a disease known as herpes zoster or shingles.

The causative agent for herpes zoster is varicella zoster virus (VZV), a double-stranded DNA virus related to the Herpes simplex virus group. Most people are infected with this virus as children, and suffer from an episode of chickenpox. The immune system eventually eliminates the virus from most locations, but it remains dormant (or latent) in the ganglia adjacent to the spinal cord (called the dorsal root ganglion) or the ganglion semilunare (ganglion Gasseri) in the base of the skull.^[1]

Herpes zoster occurs only in people who have had chickenpox, and although it can occur at any age, the majority of sufferers are more than 50 years old.^[2] The disease results from the virus reactivating in a single sensory ganglion.^[3] Chicken pox virus can remain dormant for decades, and does so inside the ganglion of the spinal cord. As the virus is reactivated it spreads down peripheral nerve fibers and produces intense pain. The blisters therefore only affect one area of the body and do not cross the midline. They are most common on the torso, but can also appear on the face, eyes or other parts of the body. In contrast to Herpes simplex virus, the latency of VZV is poorly understood. The virus has not been recovered from human nerve cells by cell culture and the location and structure of the viral DNA is not known. Virus-specific proteins continue to be made by the infected cells during the latent period, so true latency, as opposed to a chronic low-level infection, has not been proven.^[4][5] Although VZV has been detected in autopsies of nervous tissue, there are no methods to find dormant virus in the ganglia in living people.

Shingles cannot be passed from one person to another. However, the virus that causes shingles, VZV, can be spread from a person with active shingles to a person who has no immunity to the virus by direct contact with the rash, while in the blister phase. The person exposed would then develop chicken pox, not shingles. The virus is not spread through airborne transmission, such as sneezing or coughing. Once the rash has developed crusts, the person is no longer contagious. A person is not infectious before blisters appear or with post-herpetic neuralgia (pain after the rash is gone). People with active herpes zoster lesions should avoid contact with susceptible people in their household who do not have evidence of VZV immunity and in occupational settings until their lesions dry and crusted.

Unless the immune system is compromised, it suppresses reactivation of the virus and prevents herpes zoster. Why this suppression sometimes fails is poorly understood,^[6] but herpes zoster is more likely to occur in people whose immune system is impaired due to aging, immunosuppressive therapy, psychological stress, or other factors.^[7] Upon reactivation, the virus replicates in the nerve cells, and virions are shed from the cells and carried down the axons to the area of skin served by that ganglion. In the skin, the virus causes local inflammation and blisters. The short and long-term pain caused by herpes zoster comes from the widespread growth of the virus in the infected nerves, which causes inflammation.^[8]

The symptoms of herpes zoster cannot be transmitted to another person.^[9] However, during the blister phase, direct contact with the rash can spread VZV to a person who has no immunity to the virus. This newly-infected individual may then develop chickenpox, but will not immediately develop shingles. Until the rash has developed crusts, a person is extremely contagious. A person is also not infectious before blisters appear, or during postherpetic neuralgia (pain after the rash is gone). The person is no longer contagious after the virus has disappeared.^[10]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; L. Katie Morrison, MD; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Shingles can only arise in individuals who have been previously exposed to chickenpox (varicella zoster). After a person recovers from chickenpox, the virus stays in the body in a dormant (inactive) state. Herpes zoster is not caused by the same virus that causes genital herpes, a sexually transmitted disease.The disease arises from various events which depress the immune system, such as aging, severe emotional stress, severe illness, immunosuppression or long-term use of corticosteroids.^[1][2] The cellular and immunological events that lead to reactivation are poorly understood.^[3] There have been recorded cases of outbreaks occurring due to unmanaged stress or other stresses to the skin such as pinching, biting or scratching of more sensitive areas, such as nipples, ears, and underarms.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; L. Katie Morrison, MD; Associate Editor(s)-in-Chief: Varun Kumar, M.B.B.S. [2]; João André Alves Silva, M.D. [3]; Sara Mehrsefat, M.D. [4]

Diagnosis of Herpes zoster might not be possible in the absence of a rash (i.e., before rash or in cases of zoster without rash). It is sometimes confused with herpes simplex, and, occasionally, with impetigo, contact dermatitis, folliculitis, scabies, insect bites, papular urticaria, candidal infection, dermatitis herpetiformis, and drug eruptions.

Skin lesions caused by Herpes Zoster infection must be differentiated from:^{[1][2][3][4][5][6][7][8][9]}

• Depending on the location, Pain symptoms caused by Herpes Zoster infection must be differentiated from:^[1][10][11]
• Angina
• Cholecystitis
• Appendicitis
• Trigeminal neuralgia
• Renal calculi
• Glaucoma
• Spinal cord compression

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; L. Katie Morrison, MD; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Before introduction of varicella vaccine in the United States in 1995, varicella was endemic, with virtually all persons being infected by adulthood. Since implementation of the varicella vaccination program, incidence has declined in all age groups, with the greatest decline among children aged 1-4 years. Data from passive and active surveillance have indicated a decline in varicella cases of 70%-84% from 1995 through 2001 (1-3). The downward trend in varicella has continued in the United States through 2005 with an approximately 90% decline in incidence from 1995 in active surveillance sites with high vaccine coverage (CDC, unpublished data).

The incidence rate of herpes zoster ranges from 1.2 to 3.4 per 1,000 person-years among healthy individuals, increasing to 3.9–11.8 per 1,000 person‐years among those older than 65 years. ^[1] Similar incidence rates have been observed worldwide.^{[2] [3]} Herpes zoster develops in an estimated 500,000 Americans each year.^[4] Multiple studies and surveillance data demonstrate no consistent trends in incidence in the U.S. since the chickenpox vaccination program began in 1995.^[5] It is likely that incidence rate will change in the future, due to the aging of the population, changes in therapy for malignant and autoimmune diseases, and changes in chickenpox vaccination rates; a wide adoption of zoster vaccination could dramatically reduce the incidence rate.^[6] In general, herpes zoster has no seasonal incidence and does not occur in epidemics.^[7]

Most studies, but not all, suggest that the overall incidence of herpes zoster is increasing in the United States and elsewhere. This increase is independent of the effect of aging of the population. However, the rate of herpes zoster in U.S. children is declining. Children vaccinated against varicella appear to have a lower risk of reactivation of vaccine-strain VZV compared with reactivation of wild-type VZV.

Several studies report that the overall incidence of herpes zoster started increasing before the varicella vaccine was introduced in the United States. The reasons for this increase are not well understood. Currently, there is no consistent evidence that increases in herpes zoster incidence in the United States have been accelerated by the varicella vaccination program.

CDC continues to study the epidemiology of herpes zoster among adults and children and to monitor the effects of the U.S. varicella and zoster vaccination programs.

Varicella zoster virus has a high level of infectivity and is prevalent worldwide,^[8] and has a very stable prevalence from generation to generation.^[9] VZV is a benign disease in a healthy child in developed countries. However, varicella can be lethal to individuals who are infected later in life or who have low immunity. The number of people in this high-risk group has increased, due to the HIV epidemic and the increase in immunosuppressive therapies. Infections of varicella in institutions such as hospitals are also a significant problem, especially in hospitals that care for these high-risk populations.^[10]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; L. Katie Morrison, MD;Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Yamuna Kondapally, M.B.B.S[3]

Shingels are developed in patients who were previously infected with VZV (through natural infection that caused varicella or varicella vaccination).All older adults in the United States are at risk for herpes zoster as approximately 99.5% of people born in the United States who are 40 years of age and older have had varicella. Common risk factors include increasing age, immunosupression and stress.

• Shingels are developed in patients who were previously infected with VZV (through natural infection that caused varicella or varicella vaccination).^[1]
• All older adults in the United States are at risk for herpes zoster as approximately 99.5% of people born in the United States who are 40 years of age and older have had varicella.^[2]

Risk factors include:

Adults

• Previous varicella virus infection ( Varicella vaccination or varicella )
• Decline in cell mediated immunity^[3]

• Increasing age >50 yrs^[4][5]
• Immunosupression^[6][7]
  • Malignancy, especially leukemia and lymphoma
  • HIV (relative risk of herpes zoster is 15 times greater in men with HIV than a non HIV patients)^[8][9][10]
  • Organ transplant (bone marrow or solid organ transplant)^[7]
  • Medications ( steroids, chemotherapy or transplant related immunosupression medications like Bicalutamide, crofelemer, Febuxostat, Ruxolitinib, Tacrolimus, Tiagabine, Tocilizumab)^[11][12]

• Stress

Other potential risk factors include:

• Women > men^[13][14]
• Whites > African Americans (by at least 50%) ^[15].

Children

Age <10 years^[16]

• Herpes zoster is unusual in this age group except if varicella acquired during the first year of life and VZV infection in utero.

Age >10 years^[17]

• Immunosupression

• Malignancy
• Immunosupressive drugs (steroids, chemotherapy or transplant related immunosupression medications)
• HIV
• Organ transplant (bone marrow or solid organ transplant)

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sara Mehrsefat, M.D. [2]

There is no recommended screening guideline for herpes zoster.^[1]

There is no recommended screening guideline for herpes zoster.^[1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; L. Katie Morrison, MD; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]

The earliest symptoms (constituting the prodrome) of shingles include headache, sensitivity to light, fever, and malaise, all of which may be followed by itching, tingling, and pain within one to seven days.The rash and pain usually subside within 3 to 5 weeks. Many patients develop a painful condition called postherpetic neuralgia, which is often difficult to manage. Postherpetic neuralgia is most common complication of Herpes zoster.

The earliest symptoms (constituting the prodrome) of shingles include headache, sensitivity to light, fever, and malaise, all of which may be followed by itching, tingling, and pain within one to seven days. The initial phase is followed, in most cases, by development of the characteristic skin rashes of herpes zoster. The rash is visually similar to hives, and follow a distribution near dermatomes, commonly occurring in a stripe or belt-like pattern. The rash evolves into vesicles or small blisters filled with serous fluid. The vesicles are generally painful, and their development is often associated with the occurrence of anxiety and further flu-like symptoms, such as fever, tiredness, and generalized pain. The vesicles eventually become hemorrhagic (filled with blood), and crust over within seven to 10 days. As the crusts fall off, patients are rarely left with scarring and pigmented skin.

Development of the shingles rash

Day 1	Day 2	Day 5	Day 6

The rash and pain usually subside within 3 to 5 weeks. Many patients develop a painful condition called postherpetic neuralgia, which is often difficult to manage. In some patients, herpes zoster can reactivate subclinically, with pain in a dermatomal distribution without rash. This condition is known as zoster sine herpete, and may be more complicated, affecting multiple levels of the nervous system and causing multiple cranial neuropathies, polyneuritis, myelitis, or aseptic meningitis. Sometimes serious effects including partial facial paralysis (usually temporary), ear damage, or encephalitis may occur. Shingles on the upper half of the face (the first branch of the trigeminal nerve) may result in eye damage and require urgent ophthalmological assessment. Ocular complications occur in approximately one half of patients with involvement of the ophthalmic division of the trigeminal nerve.

Approximately 1 to 4% of people with herpes zoster get hospitalized for complications. Older adults and people with compromised or suppressed immune systems are more likely to get hospitalized. A study of 1994 California data found hospitalization rates of 2.1 per 100,000 person-years, rising to 9.3 per 100,000 person-years for ages 60 and up.^[1] An earlier Connecticut study found a higher hospitalization rate; the difference may be due to the prevalence of HIV in the earlier study, or to the introduction of antivirals in California before 1994.^[2] About 30% of all people hospitalized with herpes zoster are those with compromised or suppressed immune systems. A recent study estimated that there are 96 deaths each year in which herpes zoster was the actual underlying cause (0.28-0.69 per 1 million population). Almost all the deaths occurred in elderly people or those with compromised or suppressed immune systems^[3].

Since shingles is a reactivation of a virus contracted previously—often decades earlier—it cannot be induced by exposure to another person with shingles or chicken pox. Those with active blisters, however, can spread chicken pox to others who have never had that condition and who have not been vaccinated against it.^[4] Although 2nd and even 3rd episodes of herpes zoster can occur, the annual incidence of recurrence is not known. Repeated attacks of herpes zoster are rare,^[5] and it is extremely rare for patients to suffer more than three recurrences.^[6].

In one study, it was estimated that 26% of patients who contract herpes zoster eventually present with complications. Postherpetic neuralgia arises in approximately 20% of patients.^[7] Postherpetic neuralgia (PHN) is the most common complication of herpes zoster. It is a persistent pain in the area where the rash once was. PHN is diagnosed in people who have pain that persists after their rash has resolved. Some define PHN as any duration of pain after the rash resolves; others define it as duration of pain for more than 30 days, or for more than 90 days after rash onset. PHN can last for weeks or months and occasionally, for many years.

A person’s risk of having PHN after herpes zoster increases with age. Older adults are more likely to have PHN and to have longer lasting and more severe pain. Approximately 13% (and possibly more) of people 60 years of age and older with herpes zoster will get PHN. PHN is rare in people younger than 40 years old. Other predictors of PHN include the level of pain a person has when they have zoster rash and the size of their rash.

Other complications of herpes zoster include:

• Ophthalmic involvement with acute or chronic ocular sequelae (herpes zoster ophthalmicus). These complications include:^[8]
  • Mucopurulent conjunctivitis
  • Episcleritis
  • Keratitis
  • Anterior uveitis
  • Cranial nerve palsies of the third, fourth and sixth cranial nerves may occur, affecting extraocular motility.
• Bacterial superinfection of the lesions, usually due to Staphylococcus aureus and, less commonly, due to group A beta hemolytic streptococcus;
• Cranial and peripheral nerve palsies; and
• Visceral involvement, such as meningoencephalitis, pneumonitis, hepatitis, acute retinal necrosis.

People with compromised or suppressed immune systems are more likely to have complications from herpes zoster. They are more likely to have severe rash that lasts longer. Also, they are at increased risk of developing disseminated herpes zoster.

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