Introduction\ud Postnatal human cytomegalovirus (CMV) infection is usually asymptomatic in term babies, while\ud preterm infants are more susceptible to symptomatic CMV infection. Breastfeeding plays a\ud dominant role in the epidemiology of transmission of postnatal CMV infection, but the risk factors\ud of symptomatic CMV infection in preterm infants are unknown.\ud Patients and Methods\ud Between December 2003 and August 2006, eighty Very Low Birth Weight (VLBW) preterm\ud infants (gestational age ≤ 32 weeks and birth weight < 1500 g), admitted to the Neonatal Intensive\ud Care Unit of St Orsola-Malpighi General Hospital, Bologna were recruited. All of them were\ud breastfed for at least one month.\ud During the first week of life, serological test for CMV was performed on maternal blood.\ud Furthermore, urinary CMV culture was performed in all the infants in order to exclude a congenital\ud CMV infection.\ud Urine samples from each infant were collected and processed for CMV culture once a week. Once\ud every 15 days a blood sample was taken from each infant to evaluate the complete blood count, the\ud hepatic function and the C reactive protein. In addition, samples of fresh breast milk were processed\ud weekly for CMV culture. A genetic analysis of virus variant was performed in the urine of the\ud infected infants and in their mother’s milk to confirm the origin of infection.\ud Results\ud We evaluated 80 VLBW infants and their 68 mothers. Fifty-three mothers (78%) were positive for\ud CMV IgG antibodies, and 15 (22%) were seronegative.\ud In the seronegative group, CMV was never isolated in breast milk, and none of the 18 infants\ud developed viruria; in the seropositive group, CMV was isolated in 21 out of 53 (40%) mother’s\ud milk.\ud CMV was detected in the urine samples of 9 out of 26 (35%) preterm infants, who were born from\ud 21 virolactia positive mothers. Six of these infants had clinically asymptomatic CMV infection,\ud while 3 showed a sepsis-like illness with bradycardia, tachypnea and repeated desaturations. Eight\ud out of nine infants showed abnormal hematologic values.\ud The detection of neutropenia was strictly related to CMV infection (8/9 infected infants vs 17/53\ud non infected infants, P<.005), such as the detection of an increase in conjugated bilirubin (3/9\ud infected infants vs 2/53 non infected infants, P<.05). The degree of neutropenia was not different\ud between the two groups (infected/non infected).\ud The use of hemoderivatives (plasma and/or IgM–enriched immunoglobulin) in order to treat a\ud suspected/certain infection in newborn with GE< 28 ws was seen as protective against CMV\ud infection (1/4 infected infants vs 18/20 non infected infants [GE<28 ws]; P<.05).\ud Furthermore, bronchopulmonary dysplasia (defined both as oxygen-dependency at 30 days of life\ud and 36 ws of postmenstrual age) correlated with symptomatic infection (3/3 symptomatic vs 0/6\ud asymptomatic: P<.05).\ud Conclusion\ud Our data suggest that CMV infection transmitted to preterm newborn through human milk is always\ud asymptomatic when newborns are clinically stable. Otherwise, the infection can worsen a preexisting\ud disease such as bronchopulmonary dysplasia.\ud Human milk offers many nutritional and psychological advantages to preterm newborns: according\ud to our data, there’s no reason to contraindicate it neither to pasteurize the milk of all the mothers of\ud preterm infants who are CMV seropositive
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