Neurological outcomes in symptomatic congenital cytomegalovirus-infected infants after introduction of newborn urine screening and antiviral treatment.

BACKGROUND: Newborn screening for urinary cytomegalovirus (CMV) and early introduction of antiviral treatment are expected to improve neurological outcomes in symptomatic congenital CMV-infected infants. This cohort study prospectively evaluated neurological outcomes in symptomatic congenital CMV-infected infants following the introduction of hospital-based newborn urinary CMV screening and antiviral treatment. SUBJECTS/METHODS: Following institutional review board approval and written informed consent from their parents, newborns were prospectively screened from 2009 to 2014 for urinary CMV-DNA by PCR within 1 week after birth at Kobe University Hospital and affiliated hospitals. CMV-positive newborns were further examined at Kobe University Hospital, and those diagnosed as symptomatic were treated with valganciclovir for 6 weeks plus immunoglobulin. Clinical neurological outcomes were evaluated at age ⩾12 months and categorized by the presence and severity of neurologic sequelae. RESULTS: Urine samples of 6348 newborns were screened, with 32 (0.50%) positive for CMV. Of these, 16 were diagnosed with symptomatic infection and 12 received antiviral treatment. Four infants developed severe impairment (33%), three developed mild impairment (25%), and five developed normally (42%). CONCLUSIONS: This is the first Japanese report of neurological assessments in infants with symptomatic congenital CMV infection who received early diagnosis and antiviral treatment. Urinary screening, resulting in early diagnosis and treatment, may yield better neurological outcomes in symptomatic congenital CMV-infected infants.

Low total IgM values and high cytomegalovirus loads in the blood of newborns with symptomatic congenital cytomegalovirus infection.

AIMS: Neurological outcomes differ considerably between symptomatic and asymptomatic infants with congenital cytomegalovirus (CMV) infection. Our objective was to characterize laboratory markers in symptomatic newborns in comparison with asymptomatic newborns with congenital CMV infection. METHODS: Ten newborns with symptomatic and 13 newborns with asymptomatic congenital CMV infection were included in this 3-year prospective cohort study. Total immunoglobulin M (IgM), CMV-IgM, CMV antigenemia, and CMV-DNA in blood and urine were measured and their positive rates and quantitative values compared between the symptomatic and asymptomatic groups. RESULTS: Fifty percent of newborns in the symptomatic group were positive based on total IgM; this was significantly lower than in the asymptomatic group (100%). Quantitative total IgM values were significantly lower, and there were significantly more copies of CMV-DNA in the blood of symptomatic newborns than in asymptomatic newborns (median values for total IgM: 14 vs. 43 mg/dL and blood CMV-DNA: 3.2×102 vs. 3.5×101 copies/106 white blood cells). CMV-IgM, CMV antigenemia, and urine CMV-DNA did not differ significantly between groups. CONCLUSION: Low total IgM values and high blood CMV loads were associated with the presence of symptoms in newborns with congenital CMV infection.

Ureaplasma urealyticum and Mycoplasma hominis presence in umbilical cord is associated with pathogenesis of funisitis.

Ureaplasma urealyticum (U. urealyticum) and Mycoplasma hominis (M. hominis) are known to cause an intrauterine infection for preterm deliveries, but it is not known whether they are actually pathogenically involved in the development of funisitis, chorioamnionitis (CAM), and chronic lung disease (CLD) in preterm infants. Our purpose was to identify U. urealyticum and M. hominis in the umbilical cord, placenta, and tracheal aspirate (TA) or gastric fluid (GF) of preterm infants, and to clarify whether they contribute to funisitis, CAM, and CLD. Of 128 preterm infants, 86 umbilical cords, 83 placentas, and 84 TA or GF samples obtained postnatally from preterm infants were examined. U. urealyticum and M. hominis were detected by polymerase chain reaction and prospectively analyzed to determine whether the presence of U. urealyticum or M. hominis can lead to the development of funisitis, CAM, and CLD. U. urealyticum or M. hominis was isolated in nine (10.5%) of the umbilical cords, five (6.0%) of the placentas, and fifteen (17.9%) of the TA or GF samples. Funisitis was identified in all umbilical cords with U. urealyticum or M. hominis, but in only 13% of the umbilical cords without U. urealyticum and M. hominis (p < 0.001). Placentas and TA or GF with or without U. urealyticum and M. hominis did not show significant differences with regard to the development of CAM or CLD. Our results suggest that U. urealyticum and M. hominis presence is associated with the pathogenesis of funisitis, but not of CAM or CLD.