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Cytomegalovirus (CMV) remains one of the most common infections after solid organ transplantation, resulting in significant morbidity, graft loss, and occasional mortality. Management of CMV varies considerably among transplant centers. A panel of experts on CMV and solid organ transplant was convened by The Infectious Diseases Section of The Transplantation Society to develop evidence and expert opinion-based consensus guidelines on CMV management including diagnostics, immunology, prevention, treatment, drug resistance, and pediatric issues.

Cytomegalovirus (CMV) causes considerable morbidity and mortality in orthotopic liver transplant (OLT) recipients. Several prophylactic strategies against CMV have been studied in solid organ transplant recipients, including cytomegalovirus immune globulin (CMVIG). We examined the effect of CMVIG prophylaxis on first-year and long-term survival after liver transplantation. Data were analysed for 162 OLT recipients from four transplant centers in Boston who participated in two CMVIG prophylaxis trials. Ninety patients received CMVIG (median follow-up 5.6 yr), and 72 patients received placebo (median follow-up 5.4 yr). CMVIG prophylaxis was shown to be associated with increased first-year (86% vs. 72%, p = 0.029) and long-term (68% vs. 54%, p = 0.055) survival. The distribution of baseline characteristics including donor and recipient demographics, donor CMV serostatus, United Network for Organ Sharing (UNOS) status, pre-transplant renal and liver function tests, transplantation surgical time, number of units of blood products administered during transplantation, primary immunosuppressive regimen, use of solumedrol or antilymphocyte therapy for induction of immunosuppression or treatment of rejection, and surgical complications was similar for CMVIG and placebo recipients. CMVIG recipients were more likely to have primary biliary cirrhosis than placebo recipients (21% vs. 8%, p = 0.025). Using a Cox proportional hazards multivariate model to control for pre-transplant liver disease, CMVIG was shown to be independently associated with increased first-year survival (p = 0.042); a trend toward association with increased long-term survival (p = 0.098) was also shown. These data support that CMVIG prophylaxis, beyond its proven efficacy in decreasing the incidence of severe CMV-associated disease, is associated with increased survival when used prophylactically in OLT recipients.

The role of markers of cytomegalovirus (CMV) infection, such as the isolation of CMV, the presence of CMV antigenemia, or detection of viral DNA by polymerase chain reaction (PCR) assay, as predictors of subsequent CMV disease has been examined in recent studies. We studied the value of performing surveillance cultures of blood, urine, and throat specimens in a cohort of 156 liver transplant recipients who had participated in clinical trials and had received ganciclovir only for documented CMV disease. Cultures of urine and throat specimens for detection of CMV were performed every week, and cultures of blood specimens were performed every other week for the first 2 months after transplantation, then monthly for 6 months. Eighty-nine (57%) of 156 patients developed CMV infection, 41 (46%) of whom developed clinical CMV disease (36 had organ involvement and five had CMV syndrome). Fifty (32%) of 156 patients had positive blood cultures, 35 (22%) had positive urine cultures, and 41 (26%) had positive throat cultures. The positive and negative predictive values of surveillance cultures for predicting CMV disease were as follows: blood cultures, 46% and 83%, respectively; urine cultures, 26% and 74%, respectively; and throat cultures, 32% and 76%, respectively. These data indicate that such cultures are not useful in predicting CMV disease in liver transplant recipients. Future studies should examine the value of alternative markers, such as CMV antigenemia or the detection of viral DNA by PCR, for predicting CMV disease in this setting.

Primary cytomegalovirus (CMV) infection in liver transplant recipients generally occurs following transmission via a CMV-seropositive donor organ. Occasionally primary infection arises in recipients of CMV-seronegative donor organs through blood transfusions. We studied the differences in clinical manifestations of primary CMV infection associated with these two modes of transmission, among 40 liver transplant recipients who had documented primary CMV infection post-transplantation. Thirty-one of 40 patients received a CMV-seropositive donor organ; CMV infection in the other nine patients was transfusion related. Symptomatic CMV disease (22 of 31 vs. 4 of 9; P = .06), CMV hepatitis (20 of 31 vs. 1 of 9; P = .007), invasive fungal disease (13 of 31 vs. 0 of 9; P = .03), and death (16 of 31 vs. 1 of 9; P = .06) were more likely to occur in patients with donor organ-associated primary CMV infection. The incubation period between transplantation and onset of CMV infection, a possible marker for viral load, was shorter in recipients of donor organ-transmitted CMV infection (median, 44 vs. 137 days; P = .004). Controlling for potential confounders such as immunosuppression did not alter these associations. Primary CMV infection associated with the donor organ has a more profound impact than primary infection associated with transfusion. These differences may be due to dissimilarities in the viral load associated with donated livers and transfused blood products.

A case of Pneumocystis carinii pneumonia and cytomegalovirus infection occurring in a previously healthy adult male homosexual who was not receiving known immunosuppressive therapy is described. This 35-year-old man had been treated with metronidazole and tetracycline for an intermittent diarrheal illness of 5 months' duration. He was then admitted to the hospital where he was found to have a small infiltrate in the left lower lobe, and this process soon involved both lungs. Initially, Pneumocystis carinii infection and later cytomegalovirus infection were diagnosed by lung biopsy and culture. Peripheral blood lymphopenia was present and he had in vivo and in vitro abnormalities of his cellular immune responses. He was unresponsive to Bactrim as well as pentamidine and pyrimethamine therapy and died 7 wk after hospitalization.