Postnatal Cytomegalovirus Infection Research Articles

Postnatal cytomegalovirus infection and pulmonary vascular disease in extremely premature infants: A case series.

Pulmonary vascular disease (PVD) is a major determinant of both morbidity and mortality in extremely low birth weight infants. It is biologically plausible that postnatal cytomegalovirus (pCMV) infection may lead to PVD in premature infants secondary to pneumonitis or via derangement of pulmonary vascular development directly through endothelial dysfunction. Uncertainty remains, however, regarding thresholds for intervention in premature infants with cardiorespiratory instability and presumed CMV infection likely secondary to the limited understanding of the natural history of the disease. We describe four cases of premature infants with clinical and echocardiography features of PVD, in the setting of postnatally acquired CMV. All patients had atypical PVD trajectories, refractory to vasodilator treatment, which improved after initiation of CMV treatment. We highlight the need to consider postnatally acquired CMV infection in patients with PVD non-responsive to standard pulmonary vasodilator therapies or disease severity which is out of proportion of the usual clinical trajectory. Treatment of extremely premature infants with CMV-associated PVD may have positive impact on cardiorespiratory health, although duration of therapy remains uncertain.

Routine breast milk monitoring using automated molecular assay system reduced postnatal CMV infection in preterm infants.

Human cytomegalovirus (CMV) transmitted through breast milk poses fatal risks to preterm infants. However, current molecular assay systems often do not accommodate breast milk samples. In this study, we evaluated the analytical and clinical performance of the measurement procedure of CMV load in breast milk utilizing the Cobas CMV test on the Cobas 6,800 system. This was enabled by incorporating a simple independent sample preparation procedure before the application of samples on the automated assay system. Clinical data from electronic medical records were retrospectively analyzed. Breast milk samples from mothers of preterm infants born before 33 weeks of gestation were screened for CMV using the automated assay system. CMV positivity rates in breast milk and neonatal samples and the CMV transmission rate were calculated. Furthermore, to validate the analytical accuracy of the overall measurement procedure with newly obtained residual breast milk samples, the linearity of the measurement procedure was assessed, and a simplified sample preparation method was validated against a conventional method. The CMV positivity rates in maternal breast milk and neonatal samples were 57.8 and 5.2%, respectively. The CMV transmission rate through breast milk was 7.7%. No significant differences in gestational age or birth weight were found between the CMV-negative and CMV-positive neonates. The linearity of the procedure was observed within a range of 1.87-4.73 log IU/mL. The simplified sample preparation method had an equivalent or even improved CMV detection sensitivity than the conventional method. Incorporating a simple independent sample preparation procedure effectively resolved any potential issues regarding the application of breast milk on the automated assay system. Our approach contributed to reduced vertical transmission of CMV by providing a convenient and reliable method for the monitoring of breast milk CMV positivity for clinicians.

Correlates of postnatal human cytomegalovirus transmission in term babies in the first year.

Postnatal human cytomegalovirus (HCMV) infection in newborns is well characterized for preterm infants but less so for term infants. We sought to analyze the rates and routes of HCMV transmission in full-term infants during the first year of life. A cohort of 120 HCMV seropositive mothers and their 122 newborns were tested after delivery for HCMV-DNA shedding in different bodily fluids. Postnatal HCMV infection was defined as the detection of >2.5 × 102 HCMV-DNA copies/mL in infants' saliva swabs. Maternal neutralizing antibody serum titer, HCMV-specific T-cell response, and HCMV glycoprotein B immunoglobulin G on breastmilk were analyzed. HCMV shedding was detected in 67 of 120 mothers (55.8%), and 20 of 122 infants (16.4%) developed HCMV infection within the first 3 months of life. Six additional infants were infected during the first year, for a postnatal infection rate of 21.3%. Viral shedding was more frequent in breastmilk than saliva, urine, and vaginal secretions, and the mothers of infected infants showed higher levels of HCMV-DNA in milk. No association was found between the antibody levels in serum or milk and maternal viral shedding, whereas a slightly lower frequency of HCMV-specific CD4+ T-cells with long-term memory phenotype was observed in women with HCM-DNA-positive milk. About one out of five infants develop HCMV infection within the first year of life. Breastmilk appears the major route of transmission of the infection, maternal saliva has a minor role whereas the role of vaginal secretions is negligible.

The Effect of Postnatal Cytomegalovirus Infection on (Micro)structural Cerebral Development in Very Preterm Infants at Term-Equivalent Age

Introduction: There are some data indicating a negative impact of postnatal cytomegalovirus (CMV) infection on long-term neurodevelopmental outcome of preterm infants. So far, there is only little knowledge about a cerebral imaging correlate of these neurodevelopmental alterations induced by postnatal CMV infection in preterm infants. The aim of the current study was to investigate the effect of postnatal CMV infection on the incidence of brain injury and on microstructural brain maturation in very preterm infants at term-equivalent age. Methods: Infants <32 gestational weeks (02/2011–11/2018) received cerebral MRI including axial diffusion-weighted images at term-equivalent age. All infants were screened for CMV infection using urine/saliva samples, and infection was regarded as acquired postnatal if a sample became positive >5 postnatal days. We compared brain injury as well as fractional anisotropy and apparent diffusion coefficient in 14 defined cerebral regions between infants with and without postnatal CMV infection. Results: 401 infants were eligible, of whom 18 (4.5%) infants had a postnatal CMV infection. There were no significant differences in rates of brain injury or in microstructural brain development between both groups. This applied equally to the subgroup of infants <28 gestational weeks. Conclusion: Although infants with postnatal CMV infection were born more immature and more frequently suffered from complications related to immaturity, we neither observed a higher rate of preterm brain injury nor disadvantageous alterations in microstructural brain maturation at term-equivalent age.

Symptomatic Postnatal Cytomegalovirus Infection in Less than 32-Week Preterm Infants: 13-Year Retrospective Multicenter Case-Control Study

Introduction: Reports on the influence of postnatal cytomegalovirus (pCMV) infection in neonatal outcomes of preterm babies vary while guidance on management including screening is lacking. We aim to determine the association between symptomatic pCMV infection and chronic lung disease (CLD) and mortality in preterm infants born less than 32 weeks gestation. Methods: We used data from the Neonatal Intensive Care Units’ (NICUS) population-based prospective data registry of infants in 10 neonatal units in New South Wales and the Australian Capital Territory, Australia. De-identified perinatal and neonatal outcome data for 40,933 infants were examined. We identified 172 infants <32 weeks gestation with symptomatic pCMV infection. Each was matched with one control infant. Results: Infants with symptomatic pCMV infection were 2.7 times more likely to develop CLD (OR 2.7, 95% CI: 1.7–4.5) and spend 25.2 days more in hospital (95% CI: 15.2–35.2). Seventy-five percent (129/172) of infants with symptomatic pCMV were extremely preterm (<28 weeks). The mean age of symptomatic pCMV diagnosis was 62.5 ± 20.5 days or 34.7 ± 3.6 weeks-corrected gestational age. Ganciclovir treatment did not decrease CLD and death. CLD was 5.5 times predictive of death in patients with symptomatic pCMV infection. Symptomatic pCMV infection did not influence mortality nor increase neurologic impairment. Conclusion: Symptomatic pCMV is a modifiable factor affecting extreme preterm infants with significant impact on CLD. Prospective study on screening and treatment will help unveil potential benefits in our already at-risk preterm infants.

On the classification of cytomegalovirus infection in newborn children

Relevance: Cytomegalovirus (CMV) infection is the most common infection that is most commonly found in sick newborns and may be the leading cause of their morbidity and mortality. Current research and clinical observations confirm the likelihood of contracting CMV infection not only in the antenatal period but also in the perinatal and postnatal periods. The study aimed to comment on the current understanding of neonatal CMV infection, its clinical manifestations depending on the time of infection, perinatal outcomes, and long-term consequences to develop a functional classification of CMV infection in newborns. Materials and methods: A systematic review and analysis of the literature sources published by scientists in neonatology and perinatology, healthcare practitioners, and professional associations was carried out. Literature searches were conducted in PubMed, Embase, Scopus, and Euro-Peristat over the past decade by the study keywords. A total of 30 sources were included in the analysis. Results: Delayed sequelae, symptomatic and asymptomatic congenital and perinatal infections have been identified. A review shows that, to date, the incidence of asymptomatic congenital CMV infection has not been established. There is no systematization of the clinical manifestations and outcomes of congenital, perinatal, and postnatal CMV infection in newborns. Conclusion: Based on the literature review, we have developed a functional classification of CMV infection in newborns by the time of infection. Thus, CMV infection can be congenital, perinatal, or postnatal. The classification presents manifestations of symptomatic forms of CMV infection, perinatal and distant outcomes. However, there are no clear diagnostic criteria for asymptomatic forms of CMV infection. There is no clear rationale for etiopathogenetic therapy, prognostic and preventive criteria for various forms of CMV infection. All of the above tasks require further prospective cohort studies.

A case of breast milk-acquired cytomegalovirus infection in an extremely low birth weight infant.

Although breast milk is considered the optimal nutrition for infants, it is also the primary cause of postnatal cytomegalovirus (CMV) infection. Preterm infants with postnatal CMV infections are susceptible to a variety of life-threatening conditions. Twin male infants were delivered via emergency caesarian section at 27 weeks' gestation secondary to maternal complete uterine rupture. The Apgar scores at 1 and 5 min were 1 and 1 for the older twin (Twin A) and 0 and 3 for the younger twin (Twin B). Their birth weights were 1203 g (+ 0.65SD) and 495 g (- 3.79SD) respectively. On day 41, laboratory blood test results for Twin B showed a moderate elevation in C-reactive protein (CRP), thrombocytopenia. CMV quantitative polymerase chain reaction (qPCR) tests in Twin B's urine and blood as well as in the mother's breast milk were positive, but stored, dried umbilical cord CMV qPCR tests were negative. Twin B was diagnosed with a postnatal CMV infection secondary to infected breast milk and ganciclovir was commenced on day 52. Treatment was switched to valganciclovir at 74 days of age, but a negative CMV-DNA level in the blood was not achieved. Postnatal CMV infection in this infant led to an exacerbation of pre-existing bronchopulmonary dysplasia (BPD) and he demised at 182 days of age. Postnatal cytomegalovirus infections may lead to exacerbations of BPD. Early use of raw breast milk in preterm infants should be done with careful consideration of this potential complication.

Minimal adverse outcomes of postnatal cytomegalovirus infection in term or moderate and late preterm infants.

The aim of study was to investigate at what extent breastfeeding and vaginal delivery can increase mother-to-child transmission of cytomegalovirus (CMV) and to observe the clinical outcomes of postnatal infection in term or moderate and late preterm infants. In this retrospective study of prospectively collected clinical data and serum samples, during 2012-2015, 380 women with CMV IgG positive/IgM negative and their 384 infants (4 twin pairs) with gestational age ≥32 weeks were included. CMV IgG and IgM were measured with enzyme-linked immunosorbent assay. Of 384 infants followed up at 10.2 ± 2.3 months age, 177 (46.1%) were defined with CMV infection based on the presence of higher CMV IgG levels than in their mothers. The infection rate in 190 breastfed infants was higher than in 194 formula-fed infants (62.6% vs. 29.9%, P < 0.001). Vaginally delivered infants (172) had higher CMV infection rate than 212 infants delivered by caesarean section (55.2% vs. 38.7%, P = 0.001). Compared with formula feeding and caesarean section, breastfeeding and vaginal delivery increased postnatal CMV infection respectively (OR = 3.801, 95% CI 2.474-5.840, P < 0.001; OR = 1.818, 95% CI 1.182-2.796, P = 0.007). Nevertheless, compared to uninfected infants, CMV-infected infants had comparable height and body weight and showed no adverse effect on the liver enzymes. Breastfeeding and vaginal delivery can increase postnatal CMV infection; however, the infection does not influence the growth of the term infants or preterm infants with gestational age ≥32 weeks. Thus, breastfeeding should be encouraged in these infants regardless of maternal CMV IgG status.

Особенности течения постнатальной цитомегаловирусной инфекции у доношенных детей. Наблюдения из клинической практики

Cytomegalovirus infection (CMVI) is the most common viral infection in childhood. Congenital CMVI is quite well studied, always causes alertness of neonatologists, and has a diverse clinical picture after the birth of a child. Certain difficulties in diagnosis are noted in children who have postnatal CMVI. As a rule, the infection is asymptomatic or slightly symptomatic and has no special serious clinical consequences, unlike congenital CMVI, which causes hearing loss and central nervous system damage. It is known that postnatal infection is dangerous for children with impaired immune system. This risk group consists of preterm infants, mainly with very low and extremely low body weight, and full-term infants with severe concomitant congenital and/or acquired pathology. The question of infecting ways for children with postnatal CMVI remains debatable. The article also discusses the various clinical manifestations of postnatal CMVI, which can occur according to the type of CMV-related sepsis-like syndrome, hepatitis, diarrhea, neutropenia. The article highlights the importance of clear laboratory diagnostic criteria during establishing the diagnosis. There are always a lot of questions from the doctor regarding the prescription of specific treatment in CMVI and prevention methods of postnatal CMVI in full-term infants. This article also presents clinical case of postnatal CMVI in full-term infants with combined pathology receiving treatment in the conditions of the Perinatal center of St. Petersburg State Pediatric Medical University. KEYWORDS: postnatal cytomegalovirus infection, cytomegalovirus hepatitis, hearing loss, diagnosis, treatment, breast milk, neonates. FOR CITATION: Panchenko A.S., Bem E.V., Chumakova G.N., Myznikova I.V. Сourse patterns of postnatal cytomegalovirus infection in full- term infants. Cases in clinical practice. Russian Journal of Woman and Child Health. 2023;6(2):206–214 (in Russ.). DOI: 10.32364/2618- 8430-2023-6-2-206-214.

Reduced structural connectivity in non-motor networks in children born preterm and the influence of early postnatal human cytomegalovirus infection.

Preterm birth is increasingly recognized to cause lifelong functional deficits, which often show no correlate in conventional MRI. In addition, early postnatal infection with human cytomegalovirus (hCMV) is being discussed as a possible cause for further impairments. In the present work, we used fixel-based analysis of diffusion-weighted MRI to assess long-term white matter alterations associated with preterm birth and/or early postnatal hCMV infection. 36 former preterms (PT, median age 14.8 years, median gestational age 28 weeks) and 18 healthy term-born controls (HC, median age 11.1 years) underwent high angular resolution DWI scans (1.5 T, b = 2 000 s/mm2, 60 directions) as well as clinical assessment. All subjects showed normal conventional MRI and normal motor function. Early postnatal hCMV infection status (CMV+ and CMV-) had been determined from repeated screening, ruling out congenital infections. Whole-brain analysis was performed, yielding fixel-wise metrics for fiber density (FD), fiber cross-section (FC), and fiber density and cross-section (FDC). Group differences were identified in a whole-brain analysis, followed by an analysis of tract-averaged metrics within a priori selected tracts associated with cognitive function. Both analyses were repeated while differentiating for postnatal hCMV infection status. PT showed significant reductions of fixel metrics bilaterally in the cingulum, the genu corporis callosum and forceps minor, the capsula externa, and cerebellar and pontine structures. After including intracranial volume as a covariate, reductions remained significant in the cingulum. The tract-specific investigation revealed further reductions bilaterally in the superior longitudinal fasciculus and the uncinate fasciculus. When differentiating for hCMV infection status, no significant differences were found between CMV+ and CMV-. However, comparing CMV+ against HC, fixel metric reductions were of higher magnitude and of larger spatial extent than in CMV- against HC. Preterm birth can lead to long-lasting alterations of WM micro- and macrostructure, not visible on conventional MRI. Alterations are located predominantly in WM structures associated with cognitive function, likely underlying the cognitive deficits observed in our cohort. These observed structural alterations were more pronounced in preterms who suffered from early postnatal hCMV infection, in line with previous studies suggesting an additive effect.

Clinical presentation and transmission of postnatal cytomegalovirus infection in preterm infants.

Preterm infants are at greater risk of developing postnatal cytomegalovirus (CMV) infection with serious symptoms. Breast milk is the main route of CMV transmission in populations with a high seroprevalence. This study aimed to investigate the clinical presentation and transmission of postnatal CMV (pCMV) infection via breast milk in preterm infants under the specific setting of our neonatal intensive care unit (NICU). The medical records of 147 preterm infants were reviewed retrospectively, and their clinical characteristics and outcomes were analyzed. Breast milk and infant urine samples were collected every two weeks until discharge, and the kinetics of CMV loads were evaluated using a polymerase chain reaction assay. Seventeen infants (11.6%) were diagnosed with pCMV infection during the study period. In comparison between the pCMV and control groups, the mean birth weight was significantly lower in the pCMV group than in the control group (1084.1 ± 404.8 g vs. 1362.5 ± 553.8 g, P = 0.047). Four (23.5%) patients had leukocytopenia, six (35.3%) had neutropenia, three (17.6%) had thrombocytopenia, and two (11.8%) had hyperbilirubinemia in the pCMV group. Five patients were treated with antiviral agents, and their CMV load in the urine decreased after treatment. CMV loads peaked at 3-5 weeks in breast milk, whereas they peaked at 8-12 weeks of postnatal age in infants' urine. A comparison between the median CMV load in breast milk from the pCMV and control groups revealed a significant difference (P = 0.043). Most preterm infants with pCMV infection present a favorable clinical course and outcomes. A high CMV viral load in breast milk is associated with transmission. Further studies are warranted to prevent transmission and severe pCMV infections in preterm infants.

S3355 Postnatal Cytomegalovirus Infection as a Potential Trigger for Very Early Onset Crohn’s Disease in an Immunocompetent Infant

S3355 Postnatal Cytomegalovirus Infection as a Potential Trigger for Very Early Onset Crohn’s Disease in an Immunocompetent Infant

ПОСТНАТАЛЬНАЯ ЦИТОМЕГАЛОВИРУСНАЯ ИНФЕКЦИЯ У НЕДОНОШЕННОГО РЕБЕНКА: КЛИНИЧЕСКОЕ НАБЛЮДЕНИЕ

Postnatal cytomegalovirus infection (CMVI) in premature infants can have a severe, sepsis-like course with multiple organ damage. The article represents a clinical observation of overt postnatal CMVI with bilateral sialoadenitis in a child with extremely low body weight and aggravated perinatal history. The complex therapy, which included antibacterial, etiotropic (Ganciclovir) and immunoglobulin replacement therapy, has allowed the patient to recover.

Postnatal Cytomegalovirus Infection: Is it Important? A 10-Year Retrospective Case-control Study of Characteristics and Outcomes in Very Preterm and Very Low Birth Weight Infants.

To determine the characteristics and outcomes of postnatal cytomegalovirus (pCMV) infection in preterm infants in a neonatal intensive care unit (NICU). A retrospective, matched case-control study in a tertiary NICU. Infants born between January 2009 and December 2019, <32 weeks' gestational age (GA) and/or birth weight (BW) <1500 g with pCMV infection were matched 1:1 with cytomegalovirus-(CMV)-negative infants by year of admission, gender, GA and BW. Primary outcome was death ≤36 weeks' postmenstrual age or bronchopulmonary dysplasia (BPD). Secondary outcomes were length of ventilation (LOV), length of stay (LOS) and neurodevelopmental impairment (NDI) at corrected age 1 and 2 years. Forty-eight pCMV-positive infants (median GA 25.3 weeks, BW 695 g, age 58 days) were identified from 1659 infants (incidence 2.9%). The most common symptoms of pCMV infection were abdominal distension (43.8%), sepsis-like syndrome (29.2%), thrombocytopenia (60.5%) and conjugated hyperbilirubinemia (60.9%). Compared with controls, there were no significant differences in the composite outcome of death or BPD (56.3% vs. 37.5%; P = 0.1) or NDI at 1 and 2 years (51.9% vs. 44%; P = 0.8; 71.4% vs. 50%; P = 0.4). pCMV-positive infants had a significantly longer median LOV (23.5 vs. 12 days)* and LOS (140 vs. 110.5 days)*. Eleven (22.9%) infants received antivirals. Ten improved and 1 died. Two untreated infants died (1 from pCMV infection). Clinically identifiable pCMV infections are significant and associated with increased respiratory support and prolonged hospital stay in vulnerable infants. pCMV screening and preventive measures against transmission merit consideration.*P < 0.05.

Postnatal Cytomegalovirus Infection May Increase the Susceptibility of Tuberous Sclerosis Complex to Autism Spectrum Disorders.

ABSTRACTAutism spectrum disorder (ASD), a highly hereditary and heterogeneous neurodevelopmental disorder, is influenced by genetic and environmental factors. Tuberous sclerosis complex (TSC) is a common syndrome associated with ASD. Cytomegalovirus (CMV) infection is an environmental risk factor for ASD. The similarities in pathological and mechanistic pathways of TSC and CMV intrigued us to investigate whether CMV and TSC interacted in ASD’s occurrence. We detected CMV IgG seroprevalence of 308 TSC patients from our prospective cohort (September 2011 to March 2021) and 93 healthy children by magnetic particle indirect chemiluminescence immunoassay. A total of 206 TSC patients enrolled were divided into ASD and non-ASD groups, and the relationship between ASD and CMV seroprevalence was analyzed. Nested PCR and Western blot were used to detect CMV DNAs and proteins in cortical malformations of seven TSC patients with and without ASD. No difference was found in CMV seroprevalence between TSC patients and healthy children (74.0% versus 72.0%, P = 0.704). Univariate analysis showed the seroprevalence in TSC patients with ASD was higher than that in TSC patients without ASD (89.2% versus 75.1%, P = 0.063), and multifactorial analysis showed that CMV seroprevalence was a risk factor for ASD in TSC patients (OR = 3.976, 95% CI = 1.093 to 14.454). Moreover, CMV was more likely to be detected in the cortical malformations in TSC patients with ASD but not in those without ASD. The findings demonstrated that CMV may increase the susceptibility of TSC to ASD.IMPORTANCE CMV is an environmental risk factor for ASD, but its role in syndromic autism with known genetic etiology has been rarely studied. The pathogenesis of ASD is related to the interaction between environmental and genetic factors. This study demonstrated that CMV can contribute to the occurrence of ASD related to TSC, a common genetic syndrome associated with ASD. Our findings provided support for the theory of gene-environment interaction (G × E) in pathogenesis of ASD and a new perspective for the prevention and therapy for TSC related ASD.

Retinopathy of Prematurity and Possible Relation Between Postnatal Cytomegalovirus Infection.

Retinopathy of prematurity (ROP) is an eye disorder characterized by abnormal development of retinal blood vessels in premature infants. It has been associated with several risk factors, but the main factor is gestational age. Several studies have recently reported a possible link between ROP and postnatal cytomegalovirus (CMV) infection.The authors present 4 patients who developed severe ROP following postnatal CMV infection. ROP was successfully resolved with antiviral treatment in all 4 cases.Postnatal CMV infection could be responsible for the worsening of ROP. Antiviral therapy may improve the prognosis of ROP and avoid the need for more aggressive therapies.

How to Provide Breast Milk for the Preterm Infant and Avoid Symptomatic Cytomegalovirus Infection with Possible Long-Term Sequelae.

Cytomegalovirus (CMV) is able to replicate in the breast milk of lactating mothers and thus the offspring might be affected by mild to severe symptoms of postnatal CMV disease in case of prematurity; not in term infants. Sepsis-like syndrome affects only very low birth infants; and few cases have been reported. The neurodevelopmental long-term outcome of those preterm infants revealed possible subtle deficiencies, but no major neurodevelopmental impairment. Neurodevelopmental sequelae are still in discussion and seem somewhat overestimated after careful evaluation of the published evidence. The main focus of postnatal CMV disease lies upon the extremely low birth weight of infants. Elimination of CMV is provided by short-term heating methods like the most widely used Holder pasteurization. Freezing and thawing methods leave a risk for CMV acquisition. The benefits of untreated breast milk have to be considered to outweigh the possible sequelae of postnatal CMV infection in the most vulnerable preterm infants.

Incidence of congenital and postnatal cytomegalovirus infection during the first year of life in Mexican preterm infants

Cytomegalovirus infection occurs commonly during infancy. Postnatal infection in term infants is usually asymptomatic; however, infection in preterm infants can be associated with clinical manifestations during the neonatal period. Nevertheless, few studies to assess the frequency of cytomegalovirus infection in preterm infants have been performed outside of high-income countries. We analyzed the incidence of congenital and postnatal cytomegalovirus infection in a cohort of preterm infants. Cytomegalovirus infection was detected during the neonatal period in four of 178 infants; in three of them, the virus was detected during the first 3 weeks of life and, therefore, congenital infection was confirmed (1.7% incidence). Postnatal infection was detected in 44 (36.4%) of 121 infants who were assessed after discharge from the neonatal intensive care unit. Cytomegalovirus infection was significantly associated with the duration of breastfeeding. In addition, we characterized cytomegalovirus strains detected in infants together with sequences available at GenBank, based on sequences of the UL18 gene. Cytomegalovirus UL18-sequences clustered in five distinct clades (A-E), and sequences obtained from infants in our study were distributed in four of the five clades; 44.4% of these sequences were included in clade E. Breastfeeding duration was shorter on average (5.6 months) in infants with sequences in clade E compared to infants with sequences in the other three clades (8.2 months; p = .07). In conclusion, we provide information regarding the high incidence of cytomegalovirus infection in preterm infants. Further studies are warranted to assess if cytomegalovirus strain characteristics are associated with the risk of infection acquisition during infancy.

Postnatal CMV Infection and Antiviral Treatment in Extremely Premature Infants: A 12-Year Retrospective Analysis.

The impact and outcomes of postnatal cytomegalovirus (CMV) infection are not entirely clear. We aimed to determine the associations between treatment outcomes of postnatal CMV infection and its antiviral treatment. Retrospective study in a tertiary center. Infants of < 29 weeks gestational age who were tested for postnatal CMV infection were included. CMV-infected infants were compared to uninfected infants (control group). CMV-infected infants were either treated with ganciclovir and/or valganciclovir (CMVPT group) or not (CMVPNT group). Demographic, clinical, laboratory, treatment, and outcome data were collected. Primary outcomes were the length of stay, death before discharge and hearing impairment, cognitive and motor development as assessed by the Denver Developmental Screening Test II, and neurologic impairment at the corrected age of 1.5-2 years. We included 103 extremely premature infants. The Median (interquartile range [IQR]) length of stay was 94 (69-112) days in control, 85 (70-102) days in CMVPNT, and 100 (88-137) days in the CMVPT group. Mortality before discharge was 6% in control, 3.8% in CMVPNT, and 3.7% in the CMVPT group. Normal hearing at follow-up was found in 30/37 infants in control (81.1%), 13/13 infants in CMVPNT (100%), and 17/20 infants in the CMVPT group (85%). Denver Developmental Screening Test II results did not differ among the three groups. Neurologic impairment was found in 21/37 infants (56.8%) in control, 9/13 infants in CMVPNT (69.2%), and 14/20 infants in CMVPT group (70%). The associations between antiviral treatment of postnatal CMV infection and better treatment outcomes were nonsignificant.

Hearing and Neurodevelopmental Outcomes in Preterm Infants with Postnatal Cytomegalovirus Infection

Hearing and Neurodevelopmental Outcomes in Preterm Infants with Postnatal Cytomegalovirus Infection