Disseminated Adenoverus Infection in Two Premature Infants

Abstract

We present two premature infants with disseminated neonatal adenovirus infection, whose epidemiology, clinical course and outcome differ to a great extent. The first infant, born vaginally at 35 weeks gestational age after premature rupture of membranes and maternal illness, developed pneumonia, hepatitis and coagulopathy and died of circulatory failure at the age of 17 days. The other infant, delivered by cesarean section at 36 weeks gestational age, did - in contrast to all documented cases in the literature - not show any signs of pneumonia and survived meningitis without sequelae. The mode of transmission of the viral infection may have been via the maternal birth canal in the first infant and transplacental in the second one. Diagnosis was obtained by direct immunofluorescent test and serology in the first patient and by maternal serology and the detection of viral antigen in tracheal aspirates (ELISA) in the second patient. Disseminated neonatal adenovirus infection has a high mortality and should be considered in the differential diagnosis of neonatal sepsis, especially when pneumonia, hepatitis and neurologic symptoms develop together with thrombocytopenia or disseminated intravascular coagulopathy.

Fatal Disseminated Adenovirus Infections in Immunocompromised Patients

“…6,30 First described in an infant in 1964, 31 disseminated disease subsequently has been reported in patients with congenital and acquired immunodeficiency states, such as HIV infection, leukemia, bone marrow transplantation, and premature infants. [32][33][34] In the present study, all patients with disseminated adenoviral disease were immunocompromised. Possible risk factors in these patients included their underlying conditions, prolonged hospitalization, invasive procedures, broad-spectrum antibiotics, and immunosuppressive drugs.…”

Fatal adenovirus infection in a neonate and transmission to health-care workers

“…The infant's and the pediatrician's isolates were identified as HAdV9 by hemagglutination inhibition assay using mono-specific reference antisera. Molecular analysis of a partial region of the hexon gene coding hexon protein including hypervariable regions 1-6 (HVR [1][2][3][4][5][6] showed 100% nucleotide identity between the sequences from the two isolates, demonstrating viral transmission. For sequence-based typing, deduced amino acid sequences of HVR 1-6 obtained from the two clinical strains were compared with previously reported sequences and phylogenetic analysis was done using the neighborjoining method.…”

“…10 For molecular typing, deduced amino acid sequences from hexon gene demonstrated sufficient genetic divergence for molecular classification, with the exception of types HAdV15 and HAdV29, which also cannot be differentiated by antigenic method. 7 Nucleic acid and amino acid sequences for prototype strains 15 and 29 were identical over HVR [1][2][3][4][5][6] . Sequence variability on complete hexon gene between different strains of HAdV15 was in the same range as the difference between HAdV15 and HAdV29, suggesting that HAdV29 was only a variant of HAdV15.…”

Viral Respiratory Tract Infections in the Neonatal Intensive Care Unit: The VIRIoN-I Study

“…In addition, most reports on the prevalence of respiratory viral infections in NICUs have centered on outbreaks or prospective surveillance of clinically stable infants, [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15] and thus significant knowledge gaps remain. Limited data exist on their occurrence, however, because testing for viral pathogens is not performed routinely in many NICUs.…”