Introduction to Varicella (Chickenpox):
Varicella (Chickenpox) is a common and easily spread illness, especially among young children. It typically presents with a widespread rash of fluid-filled blisters affecting both the skin and mucous membranes. Most often seen in kids under the age of 10, this viral infection is known for its rapid transmission and frequent outbreaks in childhood. Adult cases do occur. It is much more common in winter and spring than in summer in temperate climates.
Epidemiology and Transmission:
Both direct contact and airborne droplets are effective ways for varicella to spread. A varicella patient is probably infectious (capable of transmitting the disease) from shortly before the appearance of rash to the first few days of rash. Because the virus usually does not enter the upper respiratory tract, contact infection is less prevalent in zoster.
Zoster patients can be the source of varicella in susceptible children. Zoster occurs sporadically, chiefly in adults and without seasonal prevalence. Usually after the age of fifty, 10 to 20 percent of adults will have at least one zoster attack in their lives. Varicella and zoster occur worldwide.
Both adults and children with impaired immune systems may have severe cases of the disease.
The symptoms of zoster (shingles), a recurrent, incapacitating illness that affects adults or people with compromised immune systems, include a rash that is restricted to the skin and innervated by a single sensory ganglion.
The lesions are similar to those of varicella. Both diseases are caused by the same virus. While zoster is the partially immune host’s reaction to the reactivation of the varicella virus, which is present in latent form in neurons in sensory ganglia, varicella is the acute illness that occurs after an initial contact with the virus.
Pathogenesis of Varicella-Zoster Virus (VZV):
The initial entry point for varicella-zoster virus (VZV) is typically the mucosal surfaces of the upper respiratory tract or the conjunctiva. After mucosal invasion, the virus undergoes its first round of replication within the draining regional lymphoid tissues. This early viral amplification gives rise to a primary viremia, allowing the virus to disseminate systemically and establish secondary replication sites, particularly within the liver and spleen.
Subsequently, secondary viremia arises as the virus-laden mononuclear cells transport VZV through the bloodstream, targeting the skin and leading to the hallmark vesicular exanthem. At the cutaneous level, viral replication provokes a series of cytopathic changes in epithelial cells, including cellular edema, ballooning degeneration, and intercellular fluid accumulation—culminating in the formation of vesicles. Host containment of viral replication is largely mediated through a coordinated humoral and cellular immune response, which restricts viral propagation and aids in recovery.
The vesicular eruptions observed in herpes zoster are histologically indistinguishable from those of primary varicella infection. However, zoster is distinguished by its pathophysiological hallmark: a robust inflammatory response within sensory neurons and associated dorsal root ganglia. Typically, reactivation is localized, involving a single sensory ganglion, with the resulting dermatomal rash aligning precisely with the cutaneous distribution of the affected nerve.
The precise molecular or immunologic triggers that prompt reactivation of latent VZV in neuronal tissues remain incompletely understood. It is postulated that a decline in VZV-specific immunity—particularly T-cell mediated surveillance—permits the virus to resume replication within neuronal cells. This reactivation initiates ganglionic inflammation and neuropathic pain, as the virus migrates centrifugally along the sensory nerve fibers to the skin, where it induces vesicular lesion formation once more.
Clinical Features and Incubation Period:
- A common disease takes 10 to 21 days to incubate.
- The incubation period of typical disease is 10–21 days.
- Malaise and fever are the earliest symptoms, soon followed by the rash, first on the trunk and then on the face, the limbs, and the buccal and pharyngeal mucosa in the mouth.
- It is possible to observe all phases of crusts, vesicles, papules, and macules simultaneously.
The majority of kids get hundreds of skin lesions, and the rash lasts roughly five days.
The viruses that cause varicella and zoster are the same; the two illnesses are caused by different reactions of the host. Lifelong immunity to varicella is thought to be conferred by prior varicella infection. The varicella vaccine produces antibodies that last for at least 20 years.
Fig: Skin lesions of Chickenpox infection
Treatment and Antiviral Therapy:
In healthy children, varicella is a mild illness that doesn’t need to be treated.
Treatment is necessary for immunocompromised people with serious infections as well as newborns.
In people exposed to varicella who are at high risk of acquiring severe disease, gammaglobulin of high varicella-zoster virus antibody titer (varicella-zoster immune globulin) can be used to prevent the sickness.
Acyclovir, valacyclovir, famciclovir, and foscarnet are among the antiviral drugs that effectively treat varicella. Acyclovir can stop the progression of zoster in adults and prevent the development of systemic disease in immunocompromised patients infected with varicella. Acyclovir does not appear to prevent post herpetic neuralgia.
Prevention and Control Measures:
A live attenuated varicella vaccine is available. Although the vaccination is only 70% effective in protecting adults from varicella, it is 80–85% successful in protecting youngsters.
The effectiveness of the vaccine in preventing serious illness is approximately 95%.