Shingles , also known as herpes zoster , is a viral disease characterized by painful skin rashes with abrasions in the local area. Usually the rash occurs in a single width line either on the left or right side of the body or face. Two to four days before the rash occurs there may be tingling or local pain in the area. If not, there are usually some symptoms although some may have fever, headache, or feel tired. The rash usually heals in two to four weeks; However, some people develop ongoing nerve pain that can last for months or years, a condition called postherpetic neuralgia. In those with poor immune function, the rash may occur widely. If the rash involves the eyes, vision loss may occur.
Herpes zoster is due to reactivation of varicella zoster virus (VZV) in a person's body. Smallpox disease is caused by initial infection with VZV. Once the chickenpox has been resolved, the virus may remain inactive in the nerve cells. When reactivated, it moves from the nervous body to the ends of the skin, producing abrasions. Risk factors for reactivation include old age, poor immune function, and have had chickenpox before the age of 18 months. How the virus stays in the body or after it is reactivated is not well understood. Exposure to virus in blisters can cause smallpox in someone who has not had it, but will not trigger a nerve rash. Diagnosis is usually based on signs and symptoms of a person. The varicella zoster virus is not the same as the herpes simplex virus; However, they belong to the same family of viruses.
Shingles vaccine reduces the risk of shingles by 50 to 90%, depending on the vaccine used. It also lowers the level of postherpetic neuralgia, and if shingles occur, its severity. If herpes zoster develops, antiviral drugs such as acyclovir can reduce the severity and duration of the illness if it begins within 72 hours after the onset of the rash. The evidence did not show any significant effect of antiviral or steroid at the postherpetic neuralgia level. Paracetamol, NSAIDs, or opioids may be used to help treat acute pain.
It is estimated that about a third of people have herpes zoster at some point in their lives. While more common among older people, children can also get sick. The number of new cases per year ranges from 1.2-3.4 per 1000 person-years between healthy people up to 3.9-11.8 per 1000 person-years among those over 65 years. About half of those living to the age of 85 will have at least one attack, and less than 5% will have more than one attack. This disease has been known since ancient times.
Video Shingles
Signs and symptoms
The earliest symptoms of herpes zoster, which include headaches, fever, and malaise, are nonspecific, and can lead to false diagnoses. These symptoms are usually followed by the sensation of burning, itching, hyperesthesia, or paresthesia ("pins and needles": tingling, stabbing, or numbness). Pain can be mild to extreme in the affected dermatome, with sensations often described as stinging, tingling, pain, numbness or throbbing, and can be interspersed with a quick stabbing pain that tortures.
Shingles in children are often painless, but people are more likely to get herpes zoster as they age, and the disease tends to be more severe.
In most cases after one to two days, but sometimes for three weeks, the initial phase is followed by the appearance of a typical skin rash. Pain and rash most commonly occur on the torso, but may appear on the face, eyes or other parts of the body. At first the rash looks similar to the first appearance of the itching; However, unlike itching, herpes zoster causes limited skin changes in dermatomes, usually resulting in a stripe or belt pattern that is limited to one side of the body and does not cross the midline. Zoster sine herpete ("zoster without herpes") describes a person who has all the symptoms of herpes zoster except this characteristic rash.
Then the rash becomes vesicular, forming small blisters filled with serous exudates, such as fever and general malaise continues. The painful vesicles eventually become turbid or dark when they are full of blood, and harden within seven to ten days; usually the crusts fall out and the skin is healed, but sometimes, after severe blistering skin, scar tissue and color change.
Face
Shingles may have additional symptoms, depending on the dermatome involved. The trigeminal nerve is the most commonly involved nerve, where the ophthalmic division is the most commonly involved branch. When the virus is reactivated in the nerve branch it is called zoster ophthalmicus . The skin of the forehead, the upper eyelid and the orbit of the eye may be involved. Zoster ophthalmicus occurs in about 10% to 25% of cases. In some people, symptoms may include conjunctivitis, keratitis, uveitis, and optic nerve palsies that can sometimes cause chronic ocular inflammation, loss of vision, and debilitating pain.
Shingles oticus , also known as Ramsay Hunt type II syndrome, involves the ear. It is estimated that the results of the virus spread from the facial nerve to the vestibulocochlear nerve. Symptoms include hearing loss and vertigo (dizziness rotation).
Shingles can occur in the mouth if the maxillary or mandibular division of the trigeminal nerve is affected, where a rash may appear on the maxillary mucosal membrane (usually the palate, occasionally upper tooth gums) or lower jaw (tongue or lower gum) respectively. Oral involvement may occur alone or in combination with a skin rash over a cutaneous distribution of the same trigeminal branch. Like shingles on the skin, lesions tend to involve only one side, distinguishing them from other conditions of the blisters. Inside the mouth, shingles initially appears as bla 1-4a (vesicles), which break down quickly to leave ulcers that heal within 10-14 days. Prodromal pain (before rash) may be confusing with toothache. Sometimes this leads to unnecessary dental care. Post herpetic neuralgia is rarely associated with herpes zoster in the mouth. Unusual complications can occur with intraoral herpes zoster not seen elsewhere. Because of the close relationship of blood vessels to the nerves, the virus can spread to involve blood vessels and compromise the blood supply, sometimes causing ischemic necrosis. Therefore, oral involvement rarely leads to complications such as osteonecrosis, tooth loss, periodontitis (gum disease), pulp calcification, pulp necrosis, periapical lesions and dental development anomalies.
Shingles deliberate
In those with poor immune function, disseminated shingle may occur (wide rash). This is defined as more than twenty skin lesions appearing outside either the dermatomes or the main affected dermatomes directly adjacent to it. In addition to the skin, other organs, such as the liver or brain, may also be affected (causing hepatitis or encephalitis), making this condition potentially lethal.
Maps Shingles
Pathophysiology
The causative agent of shingles is the varicella zoster virus (VZV) - a double-stranded DNA virus associated with the Herpes simplex virus. Most individuals are infected with this virus as children who cause chickenpox episodes. The immune system eventually removes the virus from most locations, but remains inactive (or latent) in the ganglia adjacent to the spinal cord (called the dorsal root ganglion) or the trigeminal ganglion at the base of the skull.
Herpes zoster only occurs in people who have previously been infected with VZV; although it can occur at any age, about half of cases in the United States occur in those 50 years of age or older. Recurrent herpes zoster attacks are rare, and it is very rare that a person has more than three recurrences.
The disease is caused by virus particles in a single sensory ganglion that switch from the latent lysogenic cycle to their lytic active cycle. Unlike the herpes simplex virus, the latency of VZV is poorly understood. Viruses have never been successfully recovered from human nerve cells by cell culture. A complete sequence of viral genomes was published in 1986. Specific virus proteins continued to be made by infected cells during latency periods, so latency was correct, compared with chronic, low levels, active infection, not yet proven in VZV infection. Although VZV has been detected in the autopsy of neural networks, there is no method to find a sleeping virus in living ganglia.
Unless the immune system is compromised, it suppresses virus reactivation and prevents outbreaks of herpes zoster. Why this emphasis sometimes fails to understand poorly, but shingles are more likely to occur in people whose immune systems are disturbed by aging, immunosuppressive therapy, psychological pressure, or other factors. After reactivation, the virus replicates in the body of the nerve cell, and the virion is released from the cell and carries the axon to the area of ​​skin supplied by the ganglion. In the skin, viruses cause inflammation and local blisters. The short-term and long-term pain caused by the outbreak of herpes zoster stems from the inflammation of the affected nerve due to the widespread growth of the virus in the area.
Like chickenpox and/or other forms of herpes, direct contact with an active rash may spread VZV to someone who has no immunity to the virus. These newly infected individuals can then develop chickenpox, but will not develop herpes zoster soon.
Diagnosis
If a rash has arisen, identifying the disease (making differential diagnosis) requires only visual examination, as very few diseases produce a rash on the dermatome pattern (see map). However, herpes simplex virus (HSV) can sometimes produce rashes in such patterns (zosteriform herpes simplex). Tzanck smear is helpful for diagnosing acute infection with herpes virus, but does not differentiate between HSV and VZV.
When the rash is absent (the onset or end of the disease, or in the case of sinus herpes zoster), shingles are difficult to diagnose. In addition to 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 antibodies in the blood; this only appears during smallpox or rash and not while the virus is off. In larger laboratories, the lymph collected from the blister is tested with polymerase chain reaction for VZV DNA, or examined by electron microscopy for viral particles. Molecular biology tests based on nucleic acid amplification in vitro (PCR test) are currently considered the most reliable. Nested PCR tests have high sensitivity, but are susceptible to contamination leading to false-positive results. The latest real-time PCR test is fast, easy to do, and sensitive like PCR nesting, and has a lower risk of contamination. They also have more sensitivity than viral culture.
Differential diagnosis
Herpes zoster can be mistaken for herpes simplex, dermatitis herpetiformis and impetigo, and skin reactions caused by contact dermatitis, candidiasis, certain medications and insect bites.
Prevention
There are several herpes zoster vaccines that reduce the risk of developing herpes zoster or develop severe herpes zoster if the disease occurs. They include live virus vaccines and non-live subunit vaccines.
A review by Cochrane concluded that live vaccines are useful to prevent shingles for at least three years. This equates to about 50% relative risk reduction. Vaccine reduces persistent levels, severe pain after shingles by 66% in people with herpes zoster despite vaccinations. Vaccine effectiveness is maintained through four years of follow-up. It has been recommended that people with primary or acquired immunodeficiency should not receive live vaccines.
Two doses of the adjuvanted herpes zoster subunit vaccine have a protection rate of about 90% at 3.5 years. So far it has been studied in people with complete immune system. It seems also effective at a very old age.
In the UK, Zostavax is offered to patients at the age of 70 and 78. In August 2017, just under half of the eligible 70-78 years of age have been vaccinated. About 3% of those who qualify, who have conditions that suppress their immune system, should not accept it. There are 1,104 reports of adverse reactions in April 2018.
Treatment
The goal of treatment is to limit the severity and duration of pain, shorten the duration of shingles episodes, and reduce complications. Symptomatic treatment is often necessary for postherpetic neuralgia complications. However, a study of untreated herpes zoster shows that, once the rash has healed, postherpetic neuralgia is very rare in people under 50 and fades in time; in older people the pain decreases more slowly, but even in people over 70, 85% pain free a year after their shingles outbreak.
Analgesics
People with mild to moderate pain may be treated with over-the-counter pain medications. Topical lotions containing calamine can be used on rashes or blisters and may be soothing. Sometimes, severe pain may require opioid drugs, such as morphine. After crusty lesions, capsaicin cream (Zostrix) can be used. Topical lidocaine and nerve block can also reduce pain. Gabapentin along with antivirals can offer postherpetic neuralgia assistance.
Antiviral drugs can reduce the severity and duration of herpes zoster; However, they do not prevent postherpetic neuralgia. Of these drugs, aciclovir has been the standard treatment, but new drugs of valaciclovir and famiclovir show equal or superior efficacy and good safety and tolerability. Drugs are used both for prevention (eg in HIV/AIDS) and as a therapy during the acute phase. Complications in individuals with immune disorders with shingles can be reduced with intravenous acyclovir. In people at high risk for recurrent herpes zoster attacks, five oral doses of aciclovir are usually effective.
Steroids
Corticosteroids do not appear to reduce the risk of long-term pain. But the side effects seem minimal. Its use in Ramsay Hunt syndrome has not been properly studied in 2008.
Zoster ophthalmicus
Treatment for zoster ophthalmicus is similar to standard treatment for shingles elsewhere. A recent trial comparing acyclovir with prodrug, valacyclovir, showed similar efficacy in treating this form of the disease. The significant advantage of valacyclovir versus acyclovir is its dose is only 3 times/day (compared with the dosage of aciclovir 5 times/day), which can make it more comfortable for people and improve adherence with therapy.
Prognosis
Rashes and pains usually subside within three to five weeks, but about one in five people experience a painful condition called postherpetic neuralgia, which is often difficult to manage. In some people, shingles can reactivate as zoster sine herpete : pain radiating along a single spinal cord pathway (dermatomal distribution ), but without the accompanying rash. This condition may involve complications affecting several levels of the nervous system and cause many cranial neuropathies, polyneuritis, myelitis, or aseptic meningitis. Other serious effects that may occur in some cases include partial paralysis (usually temporary), ear damage, or encephalitis. During pregnancy, the first infection with VZV, causing chicken pox, can cause fetal infection and complications in the newborn, but chronic infection or reactivation in herpes zoster is not associated with fetal infection.
There is a slight increased risk of developing cancer after a shingles infection. However, the mechanism is unclear and deaths from cancer do not seem to increase as a direct result of the presence of the virus. Conversely, an increased risk can occur due to immune suppression that allows viral reactivation.
Although shingles usually disappear within 3-5 weeks, certain complications may arise:
- Secondary bacterial infection
- Motor involvement, including weakness especially on "herpes zoster motor"
- Eye involvement: trigeminal nerve involvement (as seen in herpes ophthalmicus) should be treated early and aggressive because it can cause blindness. The involvement of the nasal tip in the zoster rash is a strong predictor of herpes ophthalmicus.
- Postherpetika neuralgia, a chronic pain condition after a nervous rash Epidemiology
- Nerves on Curlie (based on DMOZ)
- NINDS Shingles Information Page, National Institute of Neurological Disorders and Stroke
- Link to the Shingles (Hardin MD) image of the University of Iowa
- Facts About Corneal Disease and Cornea: Herpes Zoster (Shingles), National Eye Institute
Varicella zoster virus (VZV) has a high rate of infectivity and has prevalence worldwide. Herpes zoster is a re-activation of latent VZV infection: zoster can only occur in someone who previously had chickenpox (varicella).
Herpes zoster has no relationship to the seasons and does not occur in the epidemic. However, there is a strong relationship with increasing age. The incidence rate of herpes zoster ranges from 1.2-2.4 per 1,000 person-years among young healthy people, rising to 3.9-11.8 per 1000 person-years among those older than 65 years, and the rate events around the world are similar. This age-related relationship has been shown in many countries, and is associated with the fact that cellular immunity decreases with age.
Another important risk factor is immunosuppression. Other risk factors include psychological distress. According to a study in North Carolina, "black subjects were significantly less likely to develop zoster than white subjects." It is not clear whether the risks are different based on gender. Other potential risk factors include mechanical trauma and immunotoxin exposure.
There is no solid evidence for genetic links or links to family history. A 2008 study showed that people with close relatives who had herpes zoster were twice as likely to develop it themselves, but a 2010 study found no such association.
Adults with latent VZV infections exposed intermittently in children with chickenpox gain an immune boost. This periodic boost in the immune system helps prevent shingles in older adults. When routine chicken pox vaccinations are introduced in the United States, there is a concern that, since older adults will no longer receive this natural periodic boost, there will be an increase in the incidence of herpes zoster.
Some surveillance studies and data, at least when viewed superficially, show no consistent trend in incidents in the US since chickenpox vaccination programs began in 1995. However, after closer examination, two studies showed no increase in the incidence of herpes zoster done among the population. where varicella vaccination has not been widespread in the community. Further studies by Patel et al. concluded that since the introduction of chickenpox vaccine, the cost of hospitalization for herpes zoster complications has increased by more than $ 700 million per year for those over the age of 60. Another study by Yih et al . reported that as coverage of varicella vaccine in children increased, the incidence of varicella decreased, and the occurrence of shingles among adults increased by 90%. Further research results by Yawn et al . showed a 28% increase in the incidence of herpes zoster from 1996 to 2001. It is likely that the incidence rate will change in the future, due to population aging, changes in therapy for malignant and autoimmune diseases, and changes in chickenpox vaccination rates; The widespread adoption of zoster vaccination can dramatically reduce the incidence rate.
In one study, it was estimated that 26% of those with herpes zoster eventually present complications. Postherpetic neuralgia occurs in about 20% of people with shingles. A 1994 study of California data found hospitalization rates of 2.1 per 100,000 person-years, increasing to 9.3 per 100,000 person-years for age 60 and up. A previous Connecticut study found higher rates of hospitalization; the difference may be due to HIV prevalence in previous studies, or on antiviral introduction in California before 1994.
History
Herpes zoster has a long recorded history, although historical records fail to distinguish blistering caused by VZV and which are caused by smallpox, ergotism, and erysipelas. At the end of the 18th century William Heberden established a way to distinguish between herpes zoster and smallpox, and at the end of the 19th century shingles were distinguished from erysipelas. In 1831 Richard Bright hypothesized that the disease arose from the dorsal root ganglion, and a 1861 paper by Felix von BÃÆ'¤rensprung confirmed this.
The first indication that chicken pox and shingles are caused by the same virus was known at the beginning of the 20th century. Doctors began reporting that cases of shingles are often followed by smallpox in younger people who live with people with shingles. The idea of ​​a relationship between two illnesses gets stronger when it is shown that the lymph from people with shingles can cause chickenpox in young volunteers. This was eventually proved by the first isolation of the virus in cell culture, by Nobel laureate Thomas Huckle Weller, in 1953.
Until the 1940s the disease was considered benign, and serious complications were considered very rare. However, in 1942, it was recognized that herpes zoster is a more serious disease in adults than in children, and it increases in frequency with old age. Further research during the 1950s on immunosuppressed individuals showed that the disease was not as soft as ever thought, and the search for various therapeutic and preventive measures began. In the mid-1960s, several studies identified a gradual decline in cellular immunity in old age, observing that in groups of 1,000 people living up to the age of 85 years, about 500 (ie, 50%) would have at least one attack from shingles, and 10 (ie , 1%) will have at least two attacks.
In herpes zoster history research, the incidence of shingles generally increases with age. However, in his 1965 paper, Hope-Simpson suggests that "the strange age distribution of zoster may partially reflect the frequency at which different age groups are facing varicella cases and because subsequent impetus for antibody protection they have their attacks is zoster delayed". Loan support for this hypothesis that contact with children with chicken pox increases adult-mediated immunity to help delay or suppress shingles, a study by Thomas et al. reported that adults in households with children had lower rates of shingles than non-childless households. Also, a study by Terada et al. shows that pediatricians reflect incidence rates from 1/2 to 1/8 that of the general population of their age.
Etymology
The surname of all herpesviridae comes from the Greek word herpein ("spread"), referring to a latent, repetitive infection characteristic of this group of viruses. Zoster comes from the Greek z? st? r , meaning "belt" or "belt", after a typical dermatomal rash like a belt. The common name for the disease, shingles , is derived from the Latin cingulus , a variant of the Latin cingulum meaning "corset".
In Arabic the name means "belt", while in Spanish it means "little snake"; in Hindi it means "big rash" and in Norwegian its name is helvetesild , literally "fire of hell".
Research
Until the mid-1990s, the complication of central nervous system (CNS) infection caused by VZV reactivation was considered rare. The presence of a rash, as well as certain neurologic symptoms, is needed to diagnose CNS infection caused by VZV. Since 2000, PCR testing has become more widely used, and the number of diagnosed cases of CNS infection has increased.
The description of classic textbooks states that VZV reactivation in the CNS is limited to individuals who have decreased immune systems and the elderly, however, recent studies have found that the majority of patients are immunocompetent, and less than 60 years old. Older references cite vesicular rashes as characteristic findings, however, recent studies have found that rashes occur in only 45% of cases. In addition, systemic inflammation is unreliable as an indicator as previously thought: the mean level of C-reactive protein and average white blood cell counts are within the normal range in patients with VZV meningitis. MRI and CT scans are usually normal in cases of VZV reactivation in CNS. Pleositosis CSF, previously considered a strong indicator of VZV encephalitis, was absent in half of a group of patients diagnosed with VZV encephalitis by PCR.
The frequency of CNS infections presented in the community hospital emergency room can not be ignored, so there is a need to diagnose cases. PCR is not a very easy diagnostic method, but since so many other indicators are unreliable in diagnosing VZV infection on CNS, screening for VZV with PCR is recommended. Negative PCR does not rule out VZV involvement, but positive PCR can be used for diagnosis, and appropriate treatment is initiated (eg, antivirals can be prescribed rather than antibiotics).
The introduction of DNA analysis techniques has shown some complications of varicella-zoster to be more common than previously thought. For example, sporadic meningoencephalitis (ME) caused by varicella-zoster is considered a rare disease, mostly associated with childhood smallpox. However, varicella-zoster meningoencephalitis is increasingly recognized as a major cause of ME among immunocompetent adults in a non-epidemic state.
Diagnosis of varicella-zoster complications, especially in cases where the disease is active again after years or decades of latency, is difficult. The rash (rash) may be present or absent. Symptoms vary, and there is significant overlap in symptoms with herpes-simplex symptoms.
Although DNA analysis techniques such as polymerase chain reaction (PCR) can be used to look for herpes virus DNA in spinal fluid or blood, the results may be negative, even in cases where other definitive symptoms exist. Apart from these limitations, the use of PCR has resulted in progress in state of the art in our understanding of the herpes virus, including VZV, during the 1990s and 2000s. For example, in the past, doctors believed that encephalitis was caused by herpes simplex, and that the patient always died or had serious long-term problem problems. People are diagnosed on autopsies or with brain biopsies. Brain biopsy is not done lightly: it is reserved for serious cases that can not be diagnosed with a less invasive method. For this reason, knowledge of the condition of the herpes virus is limited to severe cases. DNA techniques have made it possible to diagnose "mild" cases, caused by VZV or HSV, where symptoms include fever, headache, and mental status changes. The mortality rate in treated patients decreased.
References
External links
Source of the article : Wikipedia
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