Monitoring
Post-exposure monitoring:
Patients who have been exposed to B virus should be monitored for at least 2 months despite the fact that disease onset usually occurs within 5 weeks of exposure. Patients should also receive counselling. The need for monitoring and counselling remains regardless of whether antiviral prophylaxis has been prescribed. Follow-up appointments should be scheduled to monitor for potential infection and/or disease progression. Initial appointments can be scheduled for 1, 2, and 4 weeks post-exposure, or immediately if the patient reports the development of symptoms consistent with B virus infection. For occupational exposures, the patient's supervisor at work or their occupational healthcare provider should monitor the clinical status of the patient at least weekly during the first month following exposure. During the follow-up appointments, the site of infection and the signs and symptoms of B virus infection should be evaluated. Adherence with medication should also be determined. Patients who have received post-exposure prophylaxis (PEP) should have their monitoring extended owing to the potential delay with the antibody response to B virus or suppressed viral shedding. Serological testing should be carried out again at 3 to 6 weeks following exposure; serum specimens from patients receiving PEP should be tested at later points in time (e.g., 3 months after exposure). For those patients with positive PCR or cultures from the initial wound, additional PCR or cultures may be done 1 to 2 weeks after antiviral therapy has been discontinued in order to check for viral shedding.[4]
Antiviral treatment monitoring:
Serum creatinine should be monitored in patients receiving aciclovir at high doses, and doses should be adjusted accordingly. Patients receiving ganciclovir should be closely monitored for myelosuppression.[4]
Monitoring following treatment of active disease:
Based on what is known about the pathophysiology of B virus infection and reasoning by analogy from other alphaherpesvirus infection, those who survive B virus disease are presumed to remain latently infected. The virus is presumed to persist in the peripheral nervous system (usually the nerve ganglia) for the lifetime of the host; it is not present in blood or serum of infected hosts. The virus can be detected in other body fluids (vesicular lesions, cerebrospinal fluid, oral and genital secretions) during symptomatic illness and continuing for a duration while on antiviral therapy. For these reasons, active viral shedding should be demonstrated to have stopped before intravenous antivirals are discontinued.
Monitoring for recurrence of clinical signs and symptoms suggesting recurrent active infection and for recurrence of B virus shedding is important following successful treatment of active B virus disease. Many physicians have advised a transition from intravenous antiviral therapy to ongoing oral valaciclovir or aciclovir maintenance therapy after symptoms and active virus shedding have been documented to have stopped.[4] However, there is a lack of good data on when or whether treatment should be discontinued; therefore, this should be done with expert consultation.[4]
Long-term monitoring of patients who have recovered from B virus disease should include some plan for periodic monitoring to confirm that virus shedding has not reactivated. Reactivation of treated B virus infection in survivors is rare, but at least two cases of ocular disease similar to zoster, one recurrent, have been interpreted as recurrent B virus infection.[18][38] Recurrent ocular B virus disease was treated with valaciclovir.[38]
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