Chickenpox

                                Chickenpox (varicella)

                               P.K. Ghatak, MD.

Varicella virus causes Chickenpox when a person contacts the virus for the first time. After recovery, the virus remains dormant in the nerve cells of the cranial nerve ganglia, dorsal root ganglia of the spinal cord and autonomic ganglia for the entire life of the individual. In opportune moment, the virus re-emerges and produce Zoster (Shingles) and occasionally produce more serious neurological complications. The virus called Varicella Zoster Virus (VZV)

VZV is an alpha herpesvirus. It is human herpesvirus 3 and has almost identical genomes of Simian Pox virus (SPV). Some of the pathophysiological features of VZV are similar to Cytomegalovirus.

VZV has a double-stranded DNA genome, surrounded by a nucleocapsid followed by a protein integument and a lipid envelope.

The initial infection activates cellular immune reactions followed by IgM, IgG, and IgA antibodies production. Cellular immunity provides lifelong protection.

In the USA a vaccine is routinely administered as a part of childhood vaccination, the vaccine is made from attenuated life VZV. Adults over 50 yrs of age are urged to take a second approved Zoster vaccine. This is a non-live recombinant zoster vaccine. It is given by intramuscular injection – two doses 2 to 6 months apart. It reduces the risk of herpes zoster by 92 %. The vaccine is named Shringrix and it protects vaccinated people for up to 9 years.

Clinical feature of Chickenpox.

Chickenpox infection is a common infection of childhood. It is a highly communicable disease. It is estimated that over 90 % of the world population had chickenpox. The mode of infection is by droplets and also the virus becomes airborne from a raw wound of an open vesicle. The incubation period in 10 to 15 days may be delayed to 3 weeks. The initial symptoms are cold and cough, fever, and body aches followed by erythematous skin rashes follows by papular eruptions appears the next day. The papular lesions appear first on the chest, back and then on the face followed by outwards spread to arms and legs but no lesions appear on the palms and soles. In 2 to 3 days, vesicles become embellicated and crusted. Mixed rashes consisting of papules, vesicles and crusted lesions are present at any time, which is a distinguishing feature of chickenpox from smallpox. The skin rashes are intensely itchy. In about one week, the scabs begin to fall off. From the day of onset of respiratory symptoms to crusting, all vesicles of the patient remain infectious.

Venerable population are pregnant women who did not have chickenpox before. HIV infection, cancer chemotherapy, long term steroid therapy and organ transplant patients.

Complications:

Young adult male and adult males in some instances develop orchitis, epididymitis and testicular atrophy. In a few cases, pancreatitis is reported. In rare cases, viral pneumonia can occur.

Neurological complication from Chickenpox.

The common neurological complication is cerebellititis (infection of the cerebellum). In rare cases, central vein thrombosis and stokes are recorded.

Since childhood vaccination is introduced in the USA, hardly any new chickenpox is seen. Immune status is judged by serology. It is a mandatory test for all prenatal care in the USA.

Diagnosis and Treatment:

Clinical features are distinct and since most older adults had chickenpox that helps them in diagnosis. In doubtful cases viral DNA, a specimen obtained from a vesicle, by PCR may be required.

The choice of antivirus drug is Acyclovir. The oral dose is 800 mg, given 5 times a day for 5 days.(200mg/Kg/day). Other antiviral used in Cytomegalovirus infection are also effective in chickenpox.

Varicella-Zoster Immune Globulin (VZIG):

VZIG is given as IM injection, never by IV. The therapy is a passive transfer of immunity in life-threatening situations.

Indication of VZIG.

Premature infants of immune-negative mothers. Pregnant women past 1 week of gestation with unvaccinated or negative history of previous VZV infection (seronegative). Bone marrow transplants in seronegative patents. Immune compromised patients.  Passive immunity is followed by vaccination. 

Reactivation of VZV.

Immunosuppressive conditions lead to the reactivation of VZV.  Nerve cells of all cranial nerve ganglia, Autonomic ganglion and sensory Dorsal Root Ganglion of spinal nerves are at risk of resurgence and Zoster lesions. The virus produces vasculopathy with loss of cells and focal migration of inflammatory cells and giant cell formation. This causes pain and paresthesia and loss of motor function of the dermatome the nerves supply. The pain is sharp and severe and localized to the dermatome involved and strictly limited to one side of the body. The motor fibers of the spinal are commonly effected, producing palsy (partial paralysis). The vesicles appear as bunches, like grapes, are strictly limited to the side of the body and do not cross the mid-line. Multiple dermatomes and contiguous dermatome and multiple dermatomes of different areas of the body may be involved. In some instances, no skin lesions develop, only pain is experienced.

The common places herpes zoster appear are the chest wall, followed by the face. Of the cranial nerve, the 5^th cranial nerve zoster is most common. It produces pain and vesicular lesions of one half of the face, eyelids and forehead.

In rare circumstances the virus travels to the brain and meninges via the sensory nerve from the Geniculate ganglion (ganglion of the 5th cranial nerve) producing meningoencephalitis.

Ramsay Haunt Syndrome:

Ramsay-Hunt syndrome is a special case of herpes zoster involving multiple cranial nerves. The ganglia of the 7^th,8^th, 9^th and 10^th nerves are involved. This causes severe pain, vesicular eruptions on dermatomes and mouth, tongue and throat of the area supplied by the nerves. Skin lesions appear on the external ear canal, pinna (supply by 10^th), one half of anterior 2/3rd of the tongue and soft palate and uvula. 7^th cranial nerve lesions produce lower motor neuron paralysis and stapedius muscle. 8^th cranial nerve lesion produces loss of hearing, tinnitus, nausea, vomiting, vertigo and nystagmus. 9^th and 10^th cranial nerve lesions result in paralysis of tongue, muscles of deglutition. Chorda tympani nerve lesion causes loss of taste sensation.

Diagnosis and treatment:

Clinical feature is diagnostic and confirmation if required the PCR test for viral antigen is available. The choice of  antiviral agent is Acyclovir. Other antiviral agents used in chickenpox are also effective in Zoster lesions.. In addition to viral therapy, prevention of secondary bacterial infection of the skin and mouth lesions and adequate management of pain by opioid derivates by mouth should be provided.

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