Herpes zoster, malaria, Horners syndrome Flashcards
What is the definition of Herpes Zoster (Shingles)
Herpes zoster (HZ) (shingles) is caused by reactivation of varicella-zoster virus (VZV) that was acquired during a primary varicella infection, and is characterised by dermatomal pain and papular rash.
Epidemiology of Herpes zoster
- 90% of children have been exposed to chicken pox (varicella zoster) before they are aged 16
- The annual incidence of HZ in the UK is estimated between 1.85 and 3.9 cases per 1000 population
- Herpes zoster can effect all ages but seen as a disease of the elderly
- F>M
RF of Herpes Zoster
- Increasing age
- Immunocompromise
Pathology of varicella zoster
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Varicella zoster (chicken pox):
- Varicella zoster virus is a double-stranded DNA virus, protected by a protein coat called capsid, which is enveloped in a lipid membrane.
- The virus initially enters respiratory epithelial cells - but eventually spreads to numerous cell types. It fuses with cells and releases its capsid which binds to the nucleus and injects it with viral DNA, eventually leading to the formation of capsid proteins. The newly formed virus can leave the cell (killing the cell) and cause infection.
- This can spread to other individuals via particles in the air as well as contact with oral or skin lesions
- At this point, the virus causes primary infection - chickenpox.
- Primary viremia - the virus infects a part of the immune system in the liver and spleen called the reticuloendothelial system, which is made of phagocytic cells.
- Secondary viremia - the virus starts infecting immune cells themselves, specifically T-cells. Infected T cells start expressing proteins that bind to receptors on the skin cells. At the skin, they release the virus which starts infecting keratinocytes. Sometimes the infected keratinocytes start to fuse together and create giant multinucleated cells called Tzanck cells.Uninfected cells secrete interferons alpha and beta, which protects those cells from getting infected. As a result, there are tiny lesions on the skin separated by normal areas of skin.
- The virus also infects sensory neurones in the skin, and in those neurones it travels retrogradely to the dorsal root ganglia, or if it’s on the face, the trigeminal ganglion.
- Over time, most of the viruses in the body are eliminated, but the ones in the ganglions are spared and can remain dormant for many years. The virus is now in a latent state.
Pathophysiology of Herpes Zoster
- Some remaining varicella zoster virus remains latent in the ganglion.
- If the immune system weakens, due to ageing, stress, or immunosuppressive therapy, the virus can be reactivated.
- It can then travel back up through the sensory nerve, anterogradely to the skin and cause an infection in the innervated dermatome, most commonly in lower thoracic dermatomes and ophthalmic division of trigeminal nerve.
S + S of Herpes Zoster
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Macular-vesicular rash in dermatomal distribution
- Usually in a single stripe of vesicles around either the left or the right side of the body or on one side of the face.
- Crust formation and drying occurs over the next week with resolution in 2-3 weeks
- Pain, itching, or tingling in the area where the rash is
- Malaise, myalgia, headache and fever can be present
- Disseminated infection may occur, if immunosuppressed
Investigations for Herpes Zoster
- Shingles are usually diagnosed based on clinical presentation of the skin lesions
- Diagnosis confirmed with: viral PCR, culture, immunohistochemistry
- Tzanck test: look for multinucleated giant cells in the fluid of the vesicles
- Look for varicella zoster antibodies or viral DNA.
Management of Herpes Zoster
- Oral aciclovir/ valaciclovir
- IV aciclovir if pregnant, immunosuppressed or severe/ disseminated infection
- Topical antibiotic treatment for secondary bacterial infection
- Oral/ topical analgesics
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Prevention:
- Zoster vaccine can be used to reduce zoster - not routine, but given at age 70 to prevent shingles
- VZV immunoglobulin: given if non-immune exposure in imunosuppression, pregnancy, neonates
Complications of Herpes Zoster
- Secondary bacterial infection of the lesions e.g. hepatitis, pneumonia, encephalomeningitis
- Postherpetic neuralgia: pain in the affected dermatome which lasts for more than 90 days. Affects nerve fibers and skin, causing burning pain that lasts long after the rash and blisters of shingles disappear.
- Ramsay-hunt syndrome: neurological disorder characterised by paralysis of the facial nerve (facial palsy) and a rash affecting the ear or mouth. Ear abnormalities such as ringing in the ears (tinnitus) and hearing loss may also be present.
- Herpes zoster ophthalmicus: reactivation of a varicella-zoster virus infection (shingles) involving the eye.
- Can cause chickenpox in people who have close contact
Prognosis of Herpes Zoster
Herpes zoster rarely causes fatalities in patients who are immunocompetent, but it can be life-threatening in immunocompromised patients.
Ocular complications occur in 50% to 90% of the cases, resulting in either temporary or permanently decreased visual acuity or blindness if untreated.
What is Horner’s syndrome?
triad of partial ptosis, anhidrosis over the forehead and pupillary miosis. It is caused by a Pancoast’s tumour(tumour in thepulmonary apex) pressing on thesympathetic ganglion.
What central lesions can cause Horner’s syndrome?
vascular:
- posterior inferior cerebellar artery occlusion / lateral medullary syndrome
- basilar artery occlusion
- demyelinating disease - for example multiple sclerosis
- syringomyelia or syringobulbia
- tumours
- cervical cord tumours
Pre- and post- ganglionic lesions that can cause Horner’s syndrome
- apical pulmonary disease - Pancoast’s syndrome
- cervical rib
- mediastinal tumour
- carotid aneurysm
- thyroid enlargement - goitre, tumour
- neck trauma - carotid arteriography, cervical sympathectomy
- cervical lymphadenopathy
- cervical sympathectomy
- brachial plexus lesions, for example Klumpke’s palsy
Further clinical features of Horner’s syndrome
ipsilateral miosis and partial ptosis
ipsilateral anhidria on the face
there is no enopthalmos, although the narrow palpebral aperture may suggest it
Also:
despite the ptosis - normal range of lid movement in and up and down movement - supplied by the third nerve
despite the miosis, the pupillary response to light and the near reflex are brisk and sustained but dilation of the Horner’s pupil in response to darkness is diminished or absent
the degree of miosis is not related to the level of the lesion i.e. whether central, pre- or post- ganglionic
How can we can calculate the level of a complete lesion in Horner’s syndrome using pharmacological agents?
4% cocaine eyedrops fail to dilate the pupil in Horner’s syndrome:
cocaine inhibits the reuptake of noradrenaline, if there is no noradrenaline then cocaine is inactive
hydroxyamphetamine will not dilate a Horner’s pupil if the lesion is post-ganglionic
weak adrenaline dilates a Horner’s pupil when the lesion is post-ganglionic
a normal pupil is dilated by cocaine and hydroxyamphetamine
when the lesion is pre-ganglionic only hydroxyamphetamine causes dilatation
when the lesion is post-ganglionic only adrenaline causes dilatation
