Varicella zoster

From Ganfyd

Introduction

Herpes Zoster (or Zoster, or Shingles) is a painful blistering rash owing to reactivation of the virus persisting from previous (childhood) Chickenpox, which is one of the traditionally recognised childhood exanthems.

History

• 1888 Janus Von Bokay observed varicella following contact with patients with herpes zoster^[1]
• 1907 Herpes zoster oticus described by James Ramsay Hunt.
• 1925 Zoster transmitted from shingles by Kundratitz.^[2]
• 1933 Immunological relationship betwween varicella and zoster demonstrated by Brain^[3]
• 1944 The link between Ramsay Hunt syndrome and zoster made more definite by Joseph Garland
• 1944 Transmissibility to chicken eggs from zoster lesions demonstrated by Goodpasture
• 1948 Electron microscopy showed viruses from varicella and zoster were identical in appearance^[4]
• 1952 Virus cultivated, and showed identical cytopathic changes in cell culture after inoculation with material from the vesicles of varicella and zoster
• 1958 Weller proposed the name "varicella zoster virus". ^[5]
• 1964 Hope-Simpson proposed that zoster was caused by reactivation of VZV.^{[6] [7] [8][9]}
• 1983 This was confirmed experimentally.

Isolates obtained from varicella and zoster in the same person are identical, as shown by molecular genetics since then, despite there being differences between individual strains of the Varicella Zoster virus (VZV).

Aetiology

Reactivation of Varicella zoster virus - a large DNA Herpes virus - Human Herpes Virus 3.

Clinical

A painful blistering rash, usually restricted to one or two adjacent dermatomes.

The Varicella Zoster virus (VZV) remains dormant in the Dorsal root ganglion and is reactivated, perhaps owing to stress, infection, sunlight, immunodeficiency or other intercurrent illness. This appears as a vesicular rash along the dermatome supplied by the the dorsal root nerve root. The rash tends to appear most predominately on the trunk and chest and sometimes also on the face where the eye can become involved. It can cause severe pain.

The risk of stroke is increased following an attack of shingles, especially after an attack of opththalmic shingles.^[10]

VZV in the immune suppressed

In the immune suppressed a more widespread - but often less painful - eruption may occur. Organs may also be affected. Viral shedding is more profuse and persistent.

Ophthalmic shingles

Zoster of the fifth cranial nerve is a special case and should involve a timely specialist opinion. There is a risk of blindness.

Investigations

A clinical diagnosis, although virus may be isolated from lesions.

Blood tests

Blood tests are not usually required, useful or performed.

Treatment

Medical

Varicella Zoster virus is one of the few viruses for which we have a safe effective drug available. Aciclovir and other drugs in that group are somewhat effective in attenuating the disease. Treatment is traditionally reserved for those who are believed to be at greater risk, particularly if they have a history of steroid treatment recently, but if Shingles is seen early treating it seems likely to be beneficial. The effect of anti-viral treatment of the initial illness on post-herpetic neuralgia (PHN) is unclear, although a recent review stated that:^[11]

"Meta-analyses and randomised controlled trials suggest that the oral antiviral agents aciclovir, famcicolovir, and valaciclovir started within 72 hours of the onset of rash reduce both the severity and the duration of acute pain, as well as the incidence of postherpetic neuralgia. The nucleoside analogue brivudin has been shown to be as effective as famciclovir but superior to aciclovir in both healing acute lesions and reducing postherpetic neuralgia. The pharmacokinetics of oral antivirals differ considerably, so the patient's ability to adhere to a multiple dosing regimen should be considered when selecting an agent for treatment. Antiviral treatment is effective at an early stage when viral replication is still occurring. It should be given to patients who present within 72 hours of the onset of rash and to those aged over 50 with new vesicle formation or complications whenever they present. Published guidelines advise that herpes zoster ophthalmicus should always be treated with antivirals and the advice of an ophthalmologist sought. Likewise, visceral herpes zoster requires prompt admission to hospital and use of intravenous aciclovir (10 mg/kg, eight hourly)."

(The use of the word "suggest" rather than "show" implies that the results of the studies referred to are not clear cut.)

Prevention

Although the virus is present in the blisters, shingles is minimally infectious. It can cause chickenpox - but the virus has to be inhaled or ingested. As long as the blisters can be kept covered, staff and school-children need not be excluded from work or school to prevent the infection of others. (In contrast, patients with chickenpox excrete the virus in respiratory secretions, so it can be spread by coughing.)

Immunisation

Primary infection (Chickenpox) can be safely and effectively prevented by vaccination, but the vaccine is not part of the routine UK policy - see information on chickenpox page for more details.

There is also a licensed vaccine for zoster - it's the same live attenuated virus as for varicella, but a higher concentration is used.^[12] In the USA this vaccine is recommended for everybody age 60+.^[13]

Post exposure prophylaxis

See chickenpox page.

Notification

Since shingles is a (usually late) sequela of chickenpox, there would be little point in making it notifiable. Chickenpox is not currently notifiable (although if a decision is made to move to using MMRV vaccine in the UK - as is current policy in North America - this might change).

External links and references

• BMJ "Clinical review" of Herpes zoster.^[14]
• eMedicine VZV article
• HPA Varicella zoster virus information
• Discussion on GP-UK by Michael Power Clinical Author PRODIGY Feb 2005
• History of Varicella Zoster Virus by MJ Wood ^[15]

References