RISK OF VARICELLA INFECTION

PATHOPHYSIOLOGY OF VARCICELLA INFECTION

Varicella is a nearly universal disease of children in industrialized countries:

· In these areas, only 2% of cases occur in the 15-to-49 age group.

· The incidence among pregnant women is about five per 10,000.

In tropical and subtropical countries:

· Varicella is more frequently a disease of reproductive-aged adults.

· Prenatal serologic surveys have found that 95% of US-born women are immune, compared with only 84% of those born in subtropical countries.

· Women who spent their childhood in the latter regions and subsequently moved to North America are at increased risk for varicella during pregnancy.

As with many other childhood infections, the peak incidence of VZV infection occurs in winter and spring. Attack rates for both pregnant and nonpregnant susceptible women with household contacts approach 90%. Exposures other than household contacts, such as nosocomial, school, or playmate contacts, appear somewhat less likely to result in infection. Pregnancy does not predispose a woman to acquiring the infection but may increase the risk for both mother and baby.

PATHOPHYSIOLOGY

· Primary infection occurs principally through respiratory inhalation of virus particles by a susceptible host. Direct contact with varicella or zoster lesions can also transfer the virus.

· An initial transient and asymptomatic viremia ensues, with viral propagation into the reticuloendothelial system.

· An incubation period of 10 to 21 days (mean 14 days) is followed by a second viremia, with dissemination to skin and viscera.

· Clinical evidence of infection appears within 24 to 48 hours of the second viremia.

· the virus may be transmitted to unsuspecting close contacts 1 or 2 days before the characteristic chickenpox rash is seen.

It has generally been accepted that one attack of viremia confers lifelong immunity to reinfection in patients who are not immunocompromised. Virus-specific antibodies (IgA, IgM, IgG) rise rapidly during the first 5 days of clinically apparent infection and peak at 2 to 3 weeks. Thereafter, IgG persists at lower levels. Subclinical reinfection is known to occur, however, as shown by rising antibody titers. Rarely, some patients may experience clinically apparent but mild attacks in the face of documented circulating antibody and cell-mediated immunity (CMI). Circulating antibody does not guarantee immunity, though it will ameliorate symptoms and probably prevent congenital infection. Even more rarely, VZV-immune individuals can manifest an episode of zoster after chickenpox exposure.

Before the onset of rash, adults experience fever, malaise, myalgia, and headache. Lesions then appear in crops on the face, scalp, and trunk, with relative sparing of the extremities. Initially, lesions are maculopapular, but they progress rapidly to pruritic vesicles, pustules, and scabs. New crops appear for 3 to 4 days, and crusting is generally complete within 1 week.

Characteristically, all stages of lesions will be present simultaneously. Infectivity persists until all of the vesicles become scabs; patients are therefore considered infectious from 2 days before the onset of rash until all lesions become crusted.

The overall mortality for varicella in normal adults is 50 per 100,000. Comparable data are not available for pregnant women.

Pneumonia is the most common complication of varicella in adults. Hospitalization for pneumonia is required in only 0.25% of cases of adult varicella; in those cases, however, mortality may be as high as 12% in nonpregnant and 35% in pregnant patients. Varicella pneumonia is a treacherous disease whose course can range from asymptomatic illness to sudden death. Symptoms develop 1 to 6 days after the rash appears and may consist of cough, dyspnea, fever, pleuritic chest pain, and hemoptysis. Chest auscultation often appears unremarkable, even in the face of severe pulmonary involvement. X-ray findings are not specific; they often appear as diffuse bilateral nodular infiltrates but may appear as "white out" or be interpreted as acute respiratory distress syndrome (ARDS).

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REFERENCES

1. Centers for Disease Control and Prevention. Prevention of varicella: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR. 1996;45(RR-11):1-36.

2. McGregor JA, Mark S, Crawford GP, et al. Varicella-zoster antibody testing in the care of pregnant women exposed to varicella. Am J Obstet Gynecol. 1987;157:281-284.

3. Paryani SG, Arvin AM. Intrauterine infection with varicella-zoster virus after maternal varicella. N Engl J Med. 1986;314:1542-1546.

4. Rajan P, Rivers JK. Varicella zoster virus. Recent advances in management. Can Fam Physician. 2001;47:2299-2304. Review.

5. Shields KE, Galil K, Seward J, et al. Varicella vaccine exposure during pregnancy: data from the first 5 years of the pregnancy registry. Obstet Gynecol. 2001;98:14-19.