Herpes zoster
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| Herpes zoster Classification and external resources | |
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| Herpes zoster blisters on the neck and shoulder | |
| ICD-10 | B02. |
| ICD-9 | 053 |
| DiseasesDB | 29119 |
| MedlinePlus | 000858 |
| eMedicine | med/1007 derm/180 emerg/823 oph/257 ped/996 |
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Overview
Herpes zoster, colloquially known as shingles, is the reactivation of varicella zoster virus, or VZV. The virus, one of the Herpesviridae group, leads to a group of painful blisters over the area of a dermatome.
After an attack of chicken pox, the varicella-zoster virus retreats to nerve cells within the ganglion or the spinal cord, where it will lie dormant for several months up to several decades.[1] Aging, stress, or disease will cause the varicella zoster virus to reactivate and reproduce, at which point it is known as herpes zoster. Once activated, the herpes zoster virus travels along the path of a nerve to the skin's surface, where it causes shingles.[1] [1]
Treatment is generally with antiviral drugs such as acyclovir (Zovirax), or prodrugs such as famciclovir (Famvir), or valacyclovir (Valtrex). Maximum efficacy of antiviral drugs occurs if the treatment is commenced within 72 hours of appearance of definitive symptoms.[1][1]
Nomenclature
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.
Morphology
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.
Human disease
Primary VZV infection results in chickenpox (varicella), which may rarely result in complications including VZV encephalitis or pneumonia. 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. Serious complications of shingles include post-herpetic neuralgia, zoster multiplex, myelitis, herpes ophthalmicus, or zoster sine herpete.
History
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. It was only in the late eighteenth century that William Heberden established a way to differentiate between herpes zoster and smallpox,[1] 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.[1]
Until the 1940s, the disease was considered benign, and that serious complications were thought to be very rare.[1] However, by 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. Further studies during the 1950s on immunosuppressed individuals showed that the disease was not as benign as once thought, and the search for various therapeutic and preventive measures began.[1] 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.[1]
Epidemiology
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).
Varicella zoster virus has a high level of infectivity and is prevalent worldwide,[1] and has a very stable prevalence from generation to generation.[1] 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.[1]
In general, herpes zoster has no seasonal incidence and does not occur in epidemics.[1] In temperate zones chickenpox is a disease of children, with most cases occurring during the winter and spring, most likely due to school contact; there is no evidence for regular epidemics. In the tropics chickenpox typically occurs among older people. [1] Incidence is highest in people who are over age 55, as well as in immunocompromised patients regardless of age group, and in individuals undergoing psychological stress. Non-whites may be at lower risk; it is unclear whether the risk is increased in females. Other potential risk factors include mechanical trauma, genetic susceptibility, and exposure to immunotoxins. [1]
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.[1] [1] Herpes zoster develops in an estimated 500,000 Americans each year.[1] Multiple studies and surveillance data demonstrate no consistent trends in incidence in the U.S. since the chickenpox vaccination program began in 1995.[1] 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.[1]
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.[1] 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.[1]
Pathophysiology
The causative agent for herpes zoster is varicella zoster virus (VZV). Most people are infected with this virus as a child, as it causes chicken pox. The body eliminates the virus from the system, but it remains dormant in the ganglia adjacent to the spinal cord (called the dorsal root ganglion) or the ganglion semilunare (ganglion Gasseri) in the cranial base.
Generally, the immune system suppresses reactivation of the virus. In the elderly, whose immune response generally tends to deteriorate, as well as in those patients whose immune system is being suppressed, this process fails. The virus starts replicating in the nerve cells, and newly formed viruses are carried down the axons to the area of skin served by that ganglion (a dermatome). Here, the virus causes local inflammation in the skin, with the formation of blisters.[1][1]
The pain characteristic of herpes zoster is thought to be due to irritation of the sensory nerve fibers in which the virus reproduces.[1]
Causes
Shingles can only arise in individuals who have been previously exposed to chicken pox (varicella zoster). 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][1] The cellular and immunological events that lead to reactivation are poorly understood.[1] 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.[1]
Risk Factors
Can you get chickenpox if you've been vaccinated?
Yes. About 15%–20% of people who have received one dose of chickenpox vaccine do still get chickenpox if they are exposed, but their disease is usually mild. Vaccinated persons who get chickenpox generally have fewer than 50 spots or bumps, which may resemble bug bites more than typical, fluid-filled chickenpox blisters. In 2006, the Advisory Committee on Immunization Practices (ACIP) voted to recommend routine two-dose varicella vaccination for children. In one study, children who received two doses of the chickenpox vaccine were three times less likely to get chickenpox than individuals who have had only one dose.
What are the serious complications from chickenpox?
Serious complications from chickenpox include bacterial infections which can involve many sites of the body including the skin, tissues under the skin, bone, lungs (pneumonia), joints, and blood. Other serious complications are due directly to infection with the varicella-zoster virus and include viral pneumonia, bleeding problems, and infection of the brain (encephalitis). Many people are not aware that before a vaccine was available approximately 10,600 persons were hospitalized and 100 to 150 died as a result of chickenpox in the U.S. every year.
Can a healthy person who gets varicella die from the disease?
Yes. Many of the deaths and complications from chickenpox occur in previously healthy children and adults. From 1990 to 1994, before a vaccine was available, about 50 children and 50 adults died from chickenpox every year; most of these persons were healthy or did not have a medical illness (such as cancer) that placed them at higher risk of getting severe chickenpox. Since 1999, states have been encouraged to report chickenpox deaths to CDC. These reports have shown that some deaths from chickenpox continue to occur in healthy, unvaccinated children and adults. Most of the healthy adults who died from chickenpox contracted the disease from their unvaccinated children.
Signs and symptoms
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 pain may be extreme in the affected nerve, where the rash will later develop, and can be characterized as stinging, tingling, aching, numbing, or throbbing, and can be pronounced with quick stabs of intensity. During this phase, herpes zoster is frequently misdiagnosed as other diseases with similar symptoms, including heart attacks and renal colic. Some patients may have these symptoms without developing the characteristic rash. This situation, known as "zoster sine herpete," can delay diagnosis and treatment.[1][1]
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.[1]
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).[1][1]
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.[1][1]
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What is the chickenpox illness like?
In unvaccinated children, chickenpox most commonly causes an illness that lasts about 5-10 days. Children usually miss 5 or 6 days of school or childcare due to their chickenpox and have symptoms such as high fever, severe itching, an uncomfortable rash, and dehydration or headache. In addition, about 1 in 10 unvaccinated children who get the disease will have a complication from chickenpox serious enough to visit a health-care provider. These complications include infected skin lesions, other infections, dehydration from vomiting or diarrhea, or more serious complications such as pneumonia and encephalitis. In vaccinated children, chickenpox illness is typically mild, producing no symptoms at all other than a few red bumps. However, about 25% to 30% of vaccinated children who get the disease will develop illness as serious as unvaccinated children.
Certain groups of people are more likely to have more severe illness with serious complications. These include adults, infants, adolescents, and people whose immune systems have been weakened because of illness or medications such as long-term use of steroids.
Diagnosis
If the rash has appeared, identifying this disease (making a differential diagnosis) only requires a visual examination, since very few diseases produce a rash in a dermatomal pattern (see map). However, herpes simplex virus (HSV) can occasionally produce a rash in such a pattern. The Tsanck smear is helpful for diagnosing acute infection with a herpes virus, but does not distinguish between HSV and VZV.[1]
When the rash is absent (early or late in the disease, or in the case of zoster sine herpete), herpes zoster can be difficult to diagnose.[1] Apart from the rash, most symptoms can occur also in other conditions.
Laboratory tests are available to diagnose herpes zoster. The most popular test detects VZV-specific IgM antibody in blood; this only appears during chickenpox or herpes zoster and not while the virus is dormant.[1] In larger laboratories, lymph collected from a blister is tested by the polymerase chain reaction for VZV DNA, or examined with an electron microscope for virus particles.[1]
In a recent study, samples of lesions on the skin, eyes, and lung from 182 patients with presumed herpes simplex or herpes zoster were tested with real-time PCR or with viral culture. [1]. In this comparison, viral culture detected VZV with only a 14.3% sensitivity, although the test was highly specific (specificity=100%). By comparison, real-time PCR resulted in 100% sensitivity and specificity. Overall testing for herpes simplex and herpes zoster using PCR showed a 60.4% improvement over viral culture.
Physical Examination
Skin
 Herpes zoster on the chest |
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 Varicella zoster |
 Shingles |
Treatment
Currently, there is no cure available for Herpes zoster, nor a treatment to effectively eliminate the virus from the body. However, there are some treatments that can mitigate the length of the disease and alleviate certain side effects.
Antiviral drugs
Acyclovir (an antiviral drug) inhibits replication of the viral DNA, and is used both as prophylaxis (e.g., in patients with AIDS) and as therapy for herpes zoster. Other antivirals are valacyclovir and famciclovir. During the acute phase, oral acyclovir should be given. Use of acylovir is most effective in moderating the progress of the symptoms, and in preventing post-herpetic neuralgia, if started within 24 to 72 hours of the onset of symptoms, so medical care should be obtained as soon as the condition is recognized. Immunocompromised patients may respond best to intravenous acyclovir. In patients who are at high risk for recurrences, an oral dose of acyclovir, taken twice daily, is usually effective.[1] It is also reported that the amino acid lysine inhibits the replication of herpes zoster.[1]
Other drugs
Cimetidine, a common component of over-the-counter heartburn medication, has been shown to lessen the severity of herpes zoster outbreaks in several different instances.[1][1][1] This usage is considered an off-label use of the drug. In addition, cimetidine and probenecid have been shown to reduce the renal clearance of aciclovir. [1] The study showed these compounds reduce the rate, but not the extent, at which valaciclovir is converted into aciclovir. Renal clearance of aciclovir was reduced by approximately 24% and 33% respectively. In addition, respective increases in the peak plasma concentration of acyclovir of 8% and 22% were observed. The authors concluded that these effects were "not expected to have clinical consequences regarding the safety of valaciclovir". Due to the tendency of aciclovir to precipitate in renal tubules, combining these drugs should only occur under the supervision of a physician.
Complementary Therapies
Digestive Enzymes are available on prescription and in some over the counter preparations. Before the availability of antivirals, oral pancreatic enzyme therapy in shingles was used in some countries and later subjected to clinical and scientific research. A large scale multi-centre clinical study, using an oral preparation of such enzymes, has shown promising results.[1] [1] The results of another clinical study support the concept that oral enzyme therapy is beneficial in diseases characterized in part by TGF-beta overproduction that included shingles patients. [1] TGF-β has also been found to be elevated in instances of VZV infection. [1] [1]
Prognosis
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. These complications include mucopurulent conjunctivitis, episcleritis, keratitis and anterior uveitis. Cranial nerve palsies of the third, fourth and sixth cranial nerves may occur, affecting extraocular motility.[1]
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.[1]
What are the serious complications from chickenpox?
Serious complications from chickenpox include bacterial infections which can involve many sites of the body including the skin, tissues under the skin, bone, lungs (pneumonia), joints, and blood. Other serious complications are due directly to infection with the varicella-zoster virus and include viral pneumonia, bleeding problems, and infection of the brain (encephalitis). Many people are not aware that before a vaccine was available approximately 10,600 persons were hospitalized and 100 to 150 died as a result of chickenpox in the U.S. every year.
Prevention
Zostavax is a vaccine developed by Merck & Co. which has proven successful in preventing half the cases of herpes zoster in a study of 38,000 people who received the vaccine. [1] The vaccine also reduced by two-thirds the number of cases of postherpetic neuralgia. [1] However, prior to the vaccine, it has long been known that adults received natural immune boosting from contact with children infected with varicella. This helped to suppress the reactivation of herpes zoster.[1] In Massachusetts, herpes zoster incidence increased 90%, from 2.77/1000 to 5.25/1000 in the period of increasing varicella vaccination 1999-2003.[1] The effectiveness of the varicella vaccine itself is dependent on this exogenous (outside) boosting mechanism. Thus, as natural cases of varicella decline, so has the effectiveness of the vaccine.[1]
The intake of micronutrients, including antioxidant vitamins, A, C, E and vitamin B, as well as fresh fruit, may reduce the risk of developing shingles. In one study, patients who consumed less than one serving of fruit a day had three times the risk as those who consumed over three servings per day. For those aged 60 or more, micronutrient and vegetable intake had a similar lowering of risk.[1] A recent study evaluated the effects of two types of behavioral intervention, Tai Chi and health education, on healthy adults, who, after 16 weeks of the intervention, were vaccinated with VARIVAX, a live attenuated Oka/Merck Varicella zoster virus vaccine.[1]
Primary Prevention
Varicella (Chickenpox) Vaccine can prevent this disease. Currently, two doses of vaccine are recommended for children, adolescents, and adults.
Vaccine
A live attenuated VZV Oka/Merck strain vaccine is available and is marketed under the trade name Varivax. It was developed by Merck, Sharp & Dohme in the 1980s from the Oka strain virus isolated and attenuated by Michiaki Takahashi and colleagues in the 1970s. It was submitted to the U.S. Food and Drug Administration for approval in 1990 and was approved in 1995. Since then, it has been added to the recommended vaccination schedules for children in Australia, the United States, and many other countries, causing controversy because it is only expected to be effective for about twenty years, leaving adults vulnerable to the most dangerous forms of infection by this virus. The use of varicella virus vaccine live (Varivax) has been limited by practitioner concerns that adults vaccinated as children could develop severe varicella infection complications if immunity provided by the vaccine is not long-lasting. However, clinical data has proved that the vaccine is effective for over 10 years in preventing varicella infection in healthy individuals and when breakthrough infections do occur, illness is typically mild.[1]
In 2006, the FDA approved Zostavax for the prevention of shingles. Zostavax is a more concentrated formulation of the Varivax vaccine, designed to elicit an immune response in the eldery whose immunity to VZV wanes with advancing age. [1]
References
See also
External links
- National Institute of Neurological Disorders and Stroke shingles at NINDS
- National Health Service 335
- Information about management of Shingles for physicians
- Links to pictures of Shingles (Hardin MD) University of Iowa
- After Shingles--Information about Shingles and Post-Herpetic Neuralgia
- The National Eye Institute (NEI)
- Genital Herpies Resource
- Center for Disease Control on Varicella
- Center for Disease Control on Chickenpox
- Center for Disease Control on Varicella
- Center for Disease Control on Varicella
- Center for Disease Control on Varicella
- Center for Disease Control on Shingles
da:Helvedesild
de:Herpes Zosterfr:Zona
it:Herpes zoster
he:שלבקת חוגרת
lb:Gürtelrous
nl:Gordelroos
ja:帯状疱疹
no:Helvetesildsimple:Shingles
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Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .