Etiology

Varicella is caused by primary infection with the human alpha herpes virus, varicella zoster, in a nonimmune host. Clinical disease is a manifestation of the second viremic phase of the virus. Exposure to varicella-zoster virus (VZV) initiates production of host antibodies and cell-mediated immune responses, which are important for early control and limiting dissemination of primary varicella infection. After initial presentation, the virus then establishes lifelong latency in cranial nerves and dorsal root ganglia. In up to one third of cases, VZV may reactivate later in life to produce shingles (herpes zoster).​[8]

Pathophysiology

Varicella occurs when a susceptible person is exposed to varicella-zoster virus (VZV) either by direct contact with lesions or through airborne spread from respiratory droplets.[9] After contact, the virus spreads to regional lymph nodes, resulting in a primary viremic phase. On days 4 to 6, the infection spreads to the liver, the spleen, and other cells within the reticuloendothelial system.

A secondary viremic phase occurs at about day 9, with mononuclear cells transporting the virus to the skin and mucous membranes, causing the classic vesicular rash.[10] VZV causes vasculitis of small blood vessels and degeneration of epithelial cells, leading to vesicles filled with fluid with high levels of virus.[10]

The virus is detectable in the nasopharynx 1 to 2 days before the onset of the rash, and patients are infectious at this time, before the rash develops.[11] Patients remain infectious for at least 5 days and until all lesions have crusted over. The incubation period is typically 14 days.

Classification

Clinical definitions of disease severity

Mild disease: in healthy children, the disease is generally mild and self-limited, with malaise, pruritus (itching), and temperature up to 102°F (39°C) for 2 to 3 days.

Severe disease: associated with complications such as pneumonia, neurologic sequelae, hepatitis, secondary bacterial infection, and even death.

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