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Case Reports Indian Pediatrics 2001; 38: 780-782 |
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Transfusion Transmitted CMV Infection in a Neonate |
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Piyush Gupta, Deepa Gupta, V.G. Ramachandran* , M.M.A. Faridi From
the Departments of Pediatrics and Microbiology*, University College
of Medical Sciences and Guru Teg Bahadur Hospital, Delhi 110 095, India. Manuscript
received: October 23, 2000; Initial
review completed: December 18, 2000; Cytomegalovirus (CMV) is particularly important in transfusion medicine because of the high incidence of seropositivity in the donor population and significant morbidity and mortality developing secondary to CMV seropositive blood transfusion to immunocom-promized seronegative recipients, including preterm neonates(1). However, due to lack of any national policies on CMV screening of donor blood and blood products, neonates in developing countries continue to receive seropositive blood. We seek to highlight one such incidence resulting in nosocomial trans-mission of CMV infection and the subsequent clinical syndrome. Case Report A 39-week male child was born to a primi gravida with features of intrauterine growth retardation (weight 2300 g; PI <2). The amniotic fluid was clear and there was no suggestion of perinatal asphyxia. The child was admitted to the Neonatal Intensive Care Unit at 42 hours of age with symptomatic hypoglycemia, which lasted for almost two weeks and necessitated high dose glucose infusion and steroid therapy. Despite being extensively investigated including detailed endocrine and metabolic worksup, no specific cause could be ascertained. Concurrently, the child was also detected to have hypocalcemia, early onset Staphylococcal sepsis, and un-conjugated hyperbilirubinemia, which were taken care of by appropriate therapy. Further nursery stay was complicated by nosocomial Gram-negative sepsis, meningitis and bleeding manifestations. Starvation, repeated sampling, disseminated intravascular coagulation and sepsis resulted in anemia, hypoproteinemia, and thrombocytopenia. Additionally, the child was also noticed to have cholestatic jaundice and hepato-splenomegaly from third week onwards. Conjugated hyperbilirubinemia was attributed to sepsis, as there was no bio-chemical evidence of a metabolic disease or radiological evidence of hepatobiliary obstruc-tion. Ophthalmic examination was normal. Besides, the mother was found seronegative for TORCH group of infections in the first trimester of pregnancy. During the nursery stay, the child received multiple transfusions in terms of packed red cells (days 13, 16, 23, 30, 31 and 41), fresh frozen plasma (days 17 and 34), plasma (days 16, 18 and 33), and platelet concentrate (days 14, 15 and 16). No parenteral nutrition fluids were administered. Appropriate antibiotics and supportive therapy led to amelioration of clinicals syndrome of sepsis and child could be finally discharged after 45 days of stay in the NICU. At the time of discharge, the child was feeding well though icterus and hepatospleno-megaly was persisting. Serological tests for intrauterine infection were repeated two weeks after discharge. The mother tested negative again for IgM and IgG against rubella, CMV herpes, and toxoplasma while CMV IgM titers were found elevated in the newborn. None of the other stigmata associated with CMV inclusion disease were present. The child was followed up for growth, development, icterus, hepatosplenomegaly, liver function, and CMV IgM and IgG titers; the results are summarized in Table I. Discussion CMV seropositivity in the newborn with concurrent seronegative mother as occurred in the present case can be acquired through transfusion or horizontally. The very low rate of CMV infection in newborn infants of seronegative mothers who are not exposed to other important sources such as banked human milk or seropositive blood products indicates that transmission of CMV via fomites or workers hands is very rare(2). On the other hand, the risk of neonatal CMV acquisition following transfusions of seropositive blood ranges from 12.5% in single transfusion to 25% in multiple transfusion and 50% in exchange transfusion(3). However, the entity is rarely suspected as suggested by only one report in the Indian literature(4). CMV exists in a latent state, presumable, within the leukocytes in donor blood and reactivates following transfusion, when infected cells encounter the allogenic stimulus. The virus can persist up to 4 weeks in the whole blood and almost 100 days in fresh frozen plasma. Post transfusion CMV infec-tion causes significant morbidity and mortality in premature VLBW infants born to sero-negative mothers having received multiple transfusions. These infants present with hepatosplenomegaly, atypical lymphocytosis, and thrombocytopenia resulting in 20% morta1ity. In term infants, the disease is milder and the course self-limiting as observed in the present case(5,6). Table I - Follow-up of The Child With Transfusion Transmitted CMV Infection
Preventive strategies have focussed on antibody screening of donors, leukoreduction of red cells and platelet units, antiviral agents, and immunoglobulin administration(2). While universal screening of donor blood for CMV may not be cost effective and the last two options still under research; leukoreduction techniques are being increasingly recom-mended to minimize transfusion transmitted CMV. This simple measure can help ensure that the gains achieved by increasing survival of preterm newborns in our intensive care units are not offset by increased morbidity Contributors: PG initiated and co-ordinated the case report, designed and executed the case management, and wrote the paper. He is the guarantor of the study. VGR was responsible for analysis and interpretation of virological markers. DF, VGR and MMAF helped in case analysis, discussion and interpretation of the findings, collection of reference material and writing the manuscript. Funding:
None.
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