Viral infections produce significant morbidity and mortality in the renal transplant recipient. The most common viral infections come from the herpes group of viruses: cytomegalovirus (CMV), Epstein-Barr virus (EBV), herpes simplex virus (HSV), and varicella-zoster virus (VZV). Transplant patients are also more susceptible to and have a worse outcome from infections with other viruses, such as adenovirus, influenzavirus, and hepatitis virus.
CMV is responsible for more than two-thirds of febrile episodes in the first 6 months posttransplant. Transmission of CMV occurs with an organ transplant from a seropositive donor. With the primary direct CMV infection, patients often present with fever, malaise, hepatitis, pneumonitis, primary chorioretinitis, lymphadenopathy, arthralgias, and myalgias. An important indirect effect of CMV infection is augmented immunosuppression of the host, which increases the incidence of opportunistic infections such as Pneumocystis carini, Listeria, and Aspergillus. Diagnosis of CMV infection is established by viral culture and antibody titers. Untreated CMV has been associated with 10 to 15 percent mortality rates. Intravenous ganciclovir and foscarnet are both effective in treating CMV.
EBV infection in the renal transplant patient can present in two distinct clinical syndromes, either as the typical uncomplicated mononucleosis syndrome (characterized by fever, mild hepatitis, and leukopenia with atypical lymphocytosis) or as posttransplant lymphoproliferative disease (PTLD). 8 PTLD can range from a mild benign polyclonal disease to a rapidly progressive monoclonal form, which carries a poor prognosis. Other symptoms and signs of EBV are fever of unknown origin, weight loss, hepatotoxicity, pulmonary infiltrates, and gastrointestinal bleeding and perforation. Diagnosis of EBV is established by histologic examination of infected tissue. Primary EBV infection is treated by reducing immunosuppression and administering intravenous acyclovir. Treatment of PTLD is generally ineffective, leading to a substantial mortality rate.
VZV also presents with two distinct clinical syndromes in the renal transplant patient. The majority of transplant patients with VZV present with the typical reactivation-type infection limited to skin eruptions. A primary VZV infection occurs when tissue from a seropositive donor is transplanted to a seronegative host. This primary VZV infection produces a chickenpox syndrome that can be quite virulent, causing hemorrhagic pneumonia, encephalitis, hepatitis, and pancreatitis, with a high mortality rate. Direct immunofluorescence or viral culture is required to make the diagnosis of VZV. Acyclovir, valacyclovir, and famciclovir are all effective for both primary and reactivated VZV.
HSV infection is very common during the first transplant month. The usual presentation of reactivation disease is mucocutaneous ulcerations, which can be complicated by bacterial superinfection. Primary HSV infection can present as a disseminated disease with pneumonitis, esophagitits, or hepatitis. Diagnosis is based on direct immunofluorescence, viral culture, or serologic studies. Treatment with oral or intravenous acyclovir, ganciclovir, and foscarnet is effective.
Hepatitis viruses B and C are responsible for a 10 to 15 percent incidence of chronic liver disease in transplant patients. Disease transmission is from a seropositive donor or by contact with infected individuals. Immunosuppressive therapy directly stimulates viral replication. Both hepatitis B and C can progress to active hepatitis, cirrhosis, and hepatocellular carcinoma. In addition, infection with these viruses can suppress the host's immune defenses. Diagnosis is based on serologic and histologic studies. Therapy with interferon and lamivudine has shown limited success.
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