11/14/24, 10\:44 AM Shingles

Shingles

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Shingles\: viral illness caused by reactivation of latent varicella zoster virus (VZV), characterised by a dermatomal blistering
rash.
Incidence\: 1.85-3.9 cases per 1,000 in the UK; incidence
Risk factors\: advanced age, immunosuppression (e.g. HIV, chemotherapy), malignancies, autoimmune disorders.
Symptoms\: sharp stabbing pain in a dermatome, followed by a vesicular rash; possible systemic symptoms (malaise,
headache).
Management\: aciclovir 800 mg 5x daily, famciclovir 500 mg TDS, or valaciclovir 1 g TDS for 7 days, ideally within 72 hours of
onset.
Complications\: post-herpetic neuralgia (most common), secondary bacterial infection, encephalitis, transverse myelitis,
Ramsay Hunt syndrome, Herpes zoster ophthalmicus.
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Introduction

Shingles, also known as herpes zoster, is an acute viral illness caused by the reactivation of latent varicella zoster virus
(VZV) infection. It is well known for its distinctive blistering rash, which occurs in a dermatomal distribution.
1-2
Shingles has an estimated incidence of 1.85-3.9 cases per 1,000 in the UK. It a
commonly a
2

Aetiology

VZV is one of the eight herpesviruses that a
term latent infection, prone to periodic reactivation. VZV is transmitted through aerosolised droplets and contact with
vesicular
2-3

Primary infection

Primary infection with VZV (chickenpox) typically occurs during early childhood. Following primary infection (or VZV
vaccination), a humoral response is generated which confers long-term immunity in immunocompetent individuals.
3-4

Reactivation

Once primary infection is controlled, VZV remains latent within the dorsal root and cranial ganglia. It evades the immune
system through downregulating gene expression and reducing the expression of cell surface major histocompatibility
complex antigens. Reactivation of latent infection may occur due to numerous factors such as stress, immunocompromise
or intercurrent illness.
1-2, 5
When reactivation occurs, VZV replicates within the a
the sensory nerves of the a
cutaneous symptoms within the corresponding dermatome.
2, 5
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Shingles classically a
immunosuppressed patients.
2
Figure 1. Graphic representation
of the dermatomal distribution

Risk factors

Risk factors for VZV reactivation include\:
2, 5
Advanced age (increased risk in those over 50 years old, and signi
Females
Immunosuppression (e.g. immunosuppressants, steroids, chemotherapy, HIV infection)
Malignancies (particularly haematological)
Autoimmune disorders

Clinical features

History

Shingles typically presents with 2-3 days of sharp stabbing pain in an a
rash within the same dermatome. Initially, the shingles rash is typically erythematous and macular, with vesicles appearing
within 1-2 days.
2, 5
Approximately 20% of patients will also report non-speciheadache.
2

Clinical examination

The hallmark
this rash is an important spot diagnosis.
2, 5
However, it is important to carry out a thorough examination to assess for rashes elsewhere, particularly in close proximity
to the eyes or intra-auricular rashes.
Figure 2. Shingles rash within the left T7 dermatome

Herpes zoster ophthalmicus

Herpes zoster ophthalmicus (HZO) is a variant of shingles in which the ophthalmic division (V1) of the trigeminal nerve is
acorneal ulcers, glaucoma and blindness. HZO requires
urgent administration of antivirals and an ophthalmology review.
2, 5-6

Ramsay Hunt syndrome

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Ramsay Hunt syndrome (RHS) is a form of shingles in which the geniculate ganglion of the facial nerve (CN VII) is a
RHS is characterised by the triad of otalgia, intra-auricular vesicular rash and ipsilateral facial paralysis. It is the only form
of shingles which typically presents with motor involvement.
2, 5
RHS may occasionally spread to the vestibulocochlear nerve (CN VIII), resulting in hearing loss, vertigo and tinnitus.
Facial paralysis may be the
Furthermore, stroke must be excluded in the otoscopy and screen for VZV risk factors in
unexplained facial paralysis. Unfortunately, recovery rates for facial motor dysfunction are lower for RHS compared to BP.
5
Management of RHS involves urgent antivirals and steroids. Outcomes are improved when treatment is initiated within 72
hours of onset.
2
Figure 3. Vesicular rash of Ramsay Hunt syndrome
Figure 4. Typical presentation of Ramsay Hunt syndrome
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Di

The di
1-2, 7
Contact dermatitis
Herpes simplex
Impetigo
Dermatitis herpetiformis
Autoimmune blistering disease
Candidiasis
Insect bites
Primary HIV infection
As pain typically precedes rash, shingles may initially mimic other disorders depending on the a
example, pain within the right T7 and T10 dermatomes may mimic cholecystitis or appendicitis, respectively.

Investigations

Investigations are usually not required to diagnose shingles.
Where there is uncertainty regarding the diagnosis or to di
should be obtained for polymerase chain reaction (PCR) to detect VZV DNA.
2
A viral culture of vesicular
Vesicular
immunocompromised patients.
2
HIV testing
Shingles may present due to immune dysfunction as a result of primary HIV infection. The prevalence of
undiagnosed HIV in shingles presentations is approximately 0.1%. Patients presenting with shingles should be o
a HIV test.
2

Diagnosis

Shingles is primarily a clinical diagnosis based on the characteristic features of neuralgia and vesicular rash within a well-
de
2, 5
PCR testing can be used to con

Management

Most cases of shingles are self-limiting, and treatment is mainly supportive, consisting of adequate analgesia and self-
2, 8
care.
Hospital admission should be arranged for the following groups\:
8
Evidence of HZO or visual disturbance
Immunosuppressed patients
Suspicion of CNS involvement (e.g. encephalitis, meningitis etc.)
Head or neck involvement
Disseminated zoster

Reducing transmission

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Shingles remains highly contagious until the vesicular lesions crust over, which takes approximately seven days from
onset. Until this happens, patients should be advised to avoid contact with the elderly, infants, pregnant women, the
immunocompromised, and those who are VZV naïve (i.e. never had chickenpox).
8
The rash should be kept covered while weeping as the vesicular
school or daycare if the weeping rash cannot be adequately covered.
8

Antivirals

Antivirals reduce viral replication and have been shown to reduce viral shedding and the duration of neuralgia in shingles,
as well as preventing new lesions from forming. They are most e
2, 8
Antivirals should be o
2, 8
Immunocompromised patients
Over 50 years old
Severe disease
Evidence of HZO
The recommended antivirals are\:
2, 8-11
Oral aciclovir 800 mg 5 times daily for 7 days
Oral famciclovir 500 mg 3 times daily (TDS) for 7 days
Oral valaciclovir 1 g TDS for 7 days
Intravenous antivirals should be o
immunocompromised.
Specialist opinion is required before prescribing antivirals for pregnant or breastfeeding women.

Postherpetic neuralgia

Postherpetic neuralgia (PHN) is the most common complication of shingles and describes persistent neuropathic pain in
the a
risk of PHN increases signi
2, 12-13
Paracetamol and non-steroidal anti-in
amitriptyline, duloxetine, gabapentin or pregabalin can be considered. Topical adjuncts such as capsaicin cream or
lidocaine patches may also be useful.
2, 8, 12-13
If pain is uncontrolled, referral to a pain specialist may be considered.

Prevention

Vaccination can help to reduce the risk of shingles and PHN, and is currently being expanded to include all adults aged
60-80 years old. Vaccination should also be o
2, 8
Following exposure to shingles, post-exposure prophylaxis (PEP) should be o
high risk for severe chickenpox (e.g. immunocompromised, HIV positive, pregnant).
2
PEP options include oral antivirals (oral aciclovir or valaciclovir) or intramuscular varicella-zoster immunoglobulin if antivirals
are contraindicated.
2, 9, 11

Complications

Noteworthy complications of shingles include\:
2, 5
Post-herpetic neuralgia
Herpes zoster ophthalmicus
Ramsay Hunt syndrome
Disseminated zoster
Secondary bacterial infection (of deroofed blisters)
Encephalitis
Transverse myelitis
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Guillain-Barré syndrome
VZV vasculitis

References

StatPearls. Herpes Zoster. Published in 2023. Available from\: [LINK]
BMJ Best Practice. Herpes zoster infection. Published in 2024. Available from\: [LINK]
StatPearls. Varicella-Zoster Virus (Chickenpox). Published in 2022. Available from\: [LINK]
UptoDate. Clinical features of varicella-zoster virus infection\: Chickenpox. Published in 2023. Available from\: [LINK]
UpToDate. Epidemiology, clinical manifestations, and diagnosis of herpes zoster. Published in 2022. Available from\: [LINK]
StatPearls. Herpes Zoster Ophthalmicus. Published in 2023. Available from\: [LINK]
Sampathkumar P, Drage LA, Martin DP. Herpes Zoster (Shingles) and Postherpetic Neuralgia. M a y o C l i n i c P r o c e e d i n g s .
2009 Mar;84(3)\:274–80.
NICE CKS. Shingles. Published in 2024. Available from\: [LINK]
BNF. Aciclovir. Published in 2024. Available from\: [LINK]
BNF. Famciclovir. Published in 2024. Available from\: [LINK]
BNF. Valaciclovir. Published in 2024. Available from\: [LINK]
StatPearls. Postherpetic Neuralgia. Published in 2023. Available from\: [LINK]
NICE CKS. Post-herpetic neuralgia. Published in 2024. Available from\: [LINK]

Image references

Figure 1. Goran. Dermatomes. Available from\: [LINK] License\: [CC BY-SA 4.0]
Figure 2. Hunt P. Shingles. Available from\: [LINK] License\: [CC BY 3.0]
Figure 3. Crouch A. Ramsay Hunt syndrome. Available from\: [LINK] License\: [CC BY 4.0]
Figure 4. Workman E. Ramsay Hunt syndrome. Available from\: [LINK] License\: [CC BY 4.0]

Reviewer

Dr Grant Rutledge
General Practitioner

Related notes

Chickenpox (VZV)
Clostridioides di
COVID-19
Dengue Fever
Human Immunode

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Contents

Introduction
Aetiology
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Risk factors
Clinical features
Di
Investigations
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