DIAGNOSIS OF CONGENITAL CYTOMEGALOVIRUS INFECTION BY EXAMINATION OF PLACENTA: Application of Polymerase Chain Reaction and in Situ Hybridization

We examined the placentas of 12 patients in whom congenital cytomegalovirus CMV infection was suspected from serological and or pathological evaluation. Seven patients died including four intrauterine deaths and five survived. On histological examination, the characteristic inclusion bodies were detected in only three placentas, and villitis with plasma cell infiltration was seen in eight placentas. Immunohistochemistry using a specific antibody against CMV improved the sensitivity of CMV detection 10 cases were positive . With the polymerase chain reaction PCR following the extraction of DNA from formaldehyde-fixed placenta samples, CMV DNA was detected in seven cases. All 12 subjects were diagnosed with CMV infection by additional Southern blot analysis after the PCR. CMV DNA was also detected by an in situ hybridization method in all cases. With current molecular biological techniques the placenta can be reliably used for the diagnosis of congenital CMV infection.     

Congenital cytomegalovirus infection: association between virus burden in infancy and hearing loss

OBJECTIVE: To determine the relationship between the virus burden in infancy and hearing loss in congenital CMV infection. STUDY DESIGN: A cohort of 76 infants with congenital cytomegalovirus (CMV) infection identified by means of newborn virologic screening was monitored for outcome. The amount of infectious CMV was analyzed in urine specimens obtained during early infancy. Peripheral blood (PB) samples obtained during early infancy were available from 75 children and CMV DNA was quantitated with a real-time quantitative polymerase chain reaction. RESULTS: Infants with clinical abnormalities at birth (symptomatic congenital CMV infection) had higher amounts of CMV in urine (P = .005) and CMV DNA in PB (P = .001) than infants with no symptoms. Eight children with and 4 children without symptoms had hearing loss. Among children without symptoms, those with hearing loss had a significantly greater amount of CMV in urine (P = .03) and PB virus burden (P = .02) during infancy than those with normal hearing. Infants with < 5 x 10(3) pfu/mL of urine CMV and infants with < 1 x 10(4) copies/mL of viral DNA in PB were at a lower risk for hearing loss. CONCLUSION: In children with asymptomatic congenital CMV infection, hearing loss was associated with increased amounts of urine CMV and PB CMV DNA during early infancy.     

先天性巨细胞病毒感染抗病毒治疗的效果和安全性观察

目的：观察更昔洛韦（GCV）和（或）缬更昔洛韦（VGCV）治疗先天性巨细胞病毒（ CMV）感染患儿的疗效和不良反应。 方法：回顾性纳入2012年3月1日至2017年5月31日在复旦大学附属儿科医院（我院）新生儿科住院、确诊为先天性CMV感染的患儿,随访至2017年12月31日。从病史资料中提取患儿的一般资料,抗CMV治疗的药物和疗程,新生儿期及1、 3和6月龄的肝脾触诊检查结果、胆红素和肝功能检查指标、CMV抗体和DNA检测结果、颅脑MRI、眼底检查结果和听力检测结果,治疗期间药物的不良反应。根据抗病毒治疗与否以及疗程长短分组,比较各组的临床特征和治疗反应。 结果：28例先天性CMV感染患儿进入本文分析,其中早产儿11例,男17例;无症状/轻度症状9例,未予抗病毒治疗;中重度症状19例,GCV和（或）VGCV治疗≤6周组11例,治疗6个月组8例。①6月龄时,除1例胆汁酸轻度升高外27例中枢神经系统以外的症状和体征、胆红素、肝功能和血常规均恢复正常。②无症状／轻度症状组1例在6月龄时出现左侧听力中度损失。治疗≤6周组中,2例CMV相关眼底病变于1月龄时消失; 颅脑MRI异常信号和听力损失者各5例,6月龄时分别有3例和2例无改善。治疗6个月组中,4例先天性CMV感染相关视网膜病变在随访中均消失;3例头颅MRI异常信号者和7例有听力损失者,6月龄时分别有2例和1例无改善。③治疗≤6周组和治疗6个月组在6月龄时中枢神经系统病变改善情况差异无统计学意义。④治疗过程中未发现与GCV和VGCV应用相关的粒细胞减少和肝功能异常。 结论：抗病毒治疗能改善感音神经性耳聋和脉络膜视网膜炎,GCV和（或）VGCV≤6周与6个月的治疗效果相近;建议对无临床症状先天性CMV感染患儿行眼底检查、脑干诱发电位和头颅MRI检查。     

A wider role for congenital cytomegalovirus infection in sensorineural hearing loss

BACKGROUND: Diagnostic problems in identifying congenital infection cases in infancy have thus far impaired the assessment of the role of congenital cytomegalovirus (CMV) infection in the etiology of sensorineural hearing loss (SNHL). OBJECTIVE: To estimate the impact of congenital infection in children with SNHL by detection of CMV DNA in stored samples of neonatal dried blood (dried blood spots test). METHODS: The Guthrie cards of 130 children with hearing loss >40 dB hearing loss were retrieved from the regional screening center. CMV DNA was extracted by thermal shock and amplified by PCR. RESULTS: The percentage of SNHL cases attributable to congenital CMV infection was 10% (9 of 87) in infants whose SNHL had been diagnosed in their first 2 months of life and 34.2% (13 of 38) in children with deafness of unidentified cause that was diagnosed in early childhood. In the latter group 42.7% (12 of 28) of the children with a hearing loss of >70 dB were CMV-positive. CONCLUSIONS: The results suggest that congenital CMV infection has a more relevant role in the etiology of SNHL than previously reported. The data obtained in both groups suggest that 20 to 30% of all deafness cases are caused by CMV. The percent of congenital CMV cases alone appears to account for all the cases previously attributed to all congenital infections. More than 40% of deafness cases with an unknown cause, needing rehabilitation, are caused by congenital CMV.     

Congenital cytomegalovirus infection: outcome and diagnosis

Cytomegalovirus (CMV) is the most common congenital infection in humans and an important cause of morbidity and mortality in immunocompromised hosts. Congenital CMV infection occurs in approximately 0.5 to 1 percent of all newborns in the United States and can result in significant neurological sequelae. The gold standard for diagnosing congenital CMV infection is isolation of the virus from infants within the first 2 weeks of life through conventional or rapid cell culture techniques. Newer molecular diagnostic methods to diagnose congenital CMV infection, including the nucleic acid amplification of viral DNA from the peripheral blood of infants, are being investigated, and the preliminary results show promise. However, more work must be done to standardize and validate these methods before they can be used routinely in establishing the diagnosis of congenital CMV infection.     

新生儿室管膜下囊肿的病因研究

为了探讨新生儿室管膜下囊肿（ＳＥＣ）与先天性感染的关系，采用ＥＬＩＳＡ酶标法检测母婴双方囊肿组与对照组各７０例血巨细胞病毒（ＣＭＶ）、风疹病毒、弓形虫的抗体，并应用聚合酶链反应（ＰＣＲ）技术直接检测病原ＤＮＡ（风疹病毒除外），同时作尿ＣＭＶ的ＰＣＲ检测。结果：囊肿组新生儿血ＣＭＶ－ＩｇＭ抗体和ＣＭＶ－ＰＣＲ阳性率显著高于对照组（分别为１７．１％、５．７％和１２．９％、２．９％）；且尿ＣＭＶ－ＰＣＲ的阳性率达４０．０％（２８／７０），高于对照组的１７．１％（１２／７０）；分别进行两组自身对照，尿ＣＭＶ－ＰＣＲ的阳性率显著高于血ＣＭＶ－ＰＣＲ阳性率（Ｐ＜０．０５）。囊肿组母亲的尿ＣＭＶ－ＰＣＲ阳性率亦显著高于对照组（３０％、１０％、Ｐ＜０．０１）。提示新生儿ＳＥＣ是宫内感染损害中枢神经系统的表现之一，与先天性ＣＭＶ感染有关，尿ＣＭＶ－ＰＣＲ检查可作为宫内ＣＭＶ感染的首选实验室诊断方法。     

Cytomegalovirus DNA detection on Guthrie cards in patients with neonatal cholestasis.

AIM: To time the onset of cytomegalovirus (CMV) infection in patients (n = 39) with CMV associated neonatal cholestasis by analysing CMV DNA on Guthrie cards sampled at 3 days of age. METHODS: CMV infection was diagnosed by serology/urine isolation or by CMV DNA detection (polymerase chain reaction) in liver biopsy specimens. In order to time the infection dry blood filter paper discs were punched out from stored Guthrie cards. After phenol-choloroform extraction CMV DNA was detected by nested polymerase chain reaction. RESULTS: All cards from control children (n = 8) with congenital CMV tested positive; none of the negative controls (n = 4) did so. Two of 39 cholestatic infants were CMV DNA positive; their mothers had serological signs compatible with infection during the second half of the pregnancy. All other cholestatic infants tested negative. CONCLUSIONS: CMV DNA was not detected in most of the children using Guthrie cards, suggesting that infection developed at or soon after birth.     

Unusual encephaloclastic lesions with paraventricular calcification in congenital rubella

We report an unusual case of congenital rubella. The infant was suffering from a serious encephalopathy, and both prenatal echography and neonatal CT scan showed passive ventriculomegaly with a calcified periventricular border. Usually, such lesions are strongly suggestive of cytomegalovirus (CMV) infection and have never previoulsy been reported in congenital rubella. Classic cerebral lesions in rubella are related to a prominent obstructive vasculopathy. Conversely, encephaloclastic lesions in CMV infection are likely related to a necrosis of brain parenchyma following upon an initial ventriculitis, and perhaps also to a disturbance of neuronal proliferation. Recently, Carey described a neonate with proven congenital rubella and cranial ultrasound findings typical of ventriculitis. However, in spite of the close similarity between our patient's lesions and the typical CMV lesions, we think it's impossible to assert similar pathogenic mechanisms. Actually, it's quite conceivable that only a severe or extensive vasculopathy can lead to brain atrophy with periventricular calcification in congenital rubella.     

Multicity Italian study of congenital cytomegalovirus infection

BACKGROUND: Cytomegalovirus (CMV) infection is the most frequent congenital infection in humans. Its prevalence and the frequency of disabling sequelae must be assessed in different populations to permit the formulation or assessment of preventive measures. OBJECTIVES: To check the prevalence of congenital infection and seroprevalence in Italy; to verify the rate of sensorineural hearing loss (SNHL) in infected infants; and to assess the proportion of children with SNHL attributable to congenital CMV infection. METHODS: Diagnosis of congenital CMV infection was sought in 9032 children born between March 2002 and February 2003 by testing for viral DNA [CMV dried blood spot (DBS) test] in each newborn's Guthrie card and confirmation by isolation of CMV from urine collected in the first 3 weeks of life; CMV IgG testing in 1200 women of childbearing age; clinical and audiologic tests in the first 24 months for infected children; CMV DBS tests on the Guthrie cards collected from screening centers for 77 children (3 months-5 years) presenting SNHL of 40 dB or more. RESULTS: CMV infection was diagnosed in 14 asymptomatic and 2 symptomatic newborns (0.18%). CMV seroprevalence was 80%. In 2 infected infants, transient, unilateral SNHL was found. Nineteen of the 71 children with SNHL >70 dB were congenitally infected. CONCLUSIONS: The prevalence of congenital CMV infection is low in Italy. Population characteristics limiting the circulation of CMV strains in adult women might explain this. The fact that CMV contributes to significant SNHL highlights the need for preventive measures.     

Pluripotent stem cells are protected from cytomegalovirus infection at multiple points: Implications of a new pathogenesis for congenital anomaly caused by cytomegalovirus

In humans, the cytomegalovirus (CMV) is the most significant cause of intrauterine infections that cause congenital anomalies. Intrauterine infection with human CMV is thought to be responsible for a variety of abnormalities, including mental retardation, microcephaly, developmental delay, seizure disorders, and cerebral palsy, depending on the timing of the fetal infection, the infectious route, and the virulence of the virus. In addition to the adaptive immune system, the embryo has potential resistance to CMV during early embryogenesis. Embryonic stem (ES) cells are more resistant to CMV than most other cell types, although the mechanism responsible for this resistance is not well understood. ES cells allow approximately 20-fold less murine CMV (MCMV) DNA to enter the nucleus than mouse embryonic fibroblasts (MEFs), and this inhibition occurs in a multistep manner. In situ hybridization showed that ES cell nuclei had significantly less MCMV DNA than MEF nuclei. This finding appears to be supported by the fact that ES cells express less heparan sulfate, β1-integrin, and vimentin and have fewer nuclear pores than differentiated cells such as MEF. This may reduce the ability of MCMV to attach to and enter the cellular membrane, translocate to the nucleus, and cross the nuclear membrane in pluripotent stem cells (ES-induced pluripotent stem cells). This finding may indicate a new pathogenesis for the congenital anomaly caused by CMV.     

Congenital cytomegalovirus infection in preterm and full-term newborn infants from a population with a high seroprevalence rate

BACKGROUND: Cytomegalovirus (CMV) is the most frequent cause of congenital infections in humans. Prematurity occurs in as many as 34% of infants with symptomatic congenital CMV infection. OBJECTIVE: To determine the clinical presentation and frequency of congenital CMV infection among preterm infants and full-term infants from a population with a high seroprevalence rate. DESIGN/METHODS: A total of 289 preterm infants (median gestational age, 34 weeks; median birth weight, 1,757 g) and 163 term infants (median gestational age, 39 weeks; median birth weight, 3,150 g) sequentially born were included in the study. Serum IgG antibodies to CMV were measured in all mothers. One urine sample was collected within the first 7 days of age from all newborns. Virus isolation in urine samples was performed by tissue culture, and viral DNA was detected by a multiplex PCR. CMV infection was diagnosed in infants with virus excretion detected by both methods on at least two occasions within the first 3 weeks of life. RESULTS: Maternal CMV seropositivity rate was 95.7%. Congenital CMV infection was detected in 6 of 289 (2.1%) (95% confidence interval, 0.84 to 4.68) preterm infants and in 3 of 163 term infants (1.8%) (95% confidence interval, 0.48 to 5.74) (P > 0.05). Four of 6 preterm infants with congenital CMV infection were symptomatic, but none of the term infants was symptomatic (P = 0.16). CONCLUSION: The frequency of congenital CMV infection in preterm newborn infants from mothers with a high seropositive rate was similar to that found in term infants. No significant difference was found between the proportion of symptomatic infants among preterm and term infants. Our finding of symptomatic congenital CMV infection underscores the need of further evaluation of correlates of congenital symptomatic infection in highly immune populations.     

No CMV DNA in Guthrie cards from children who later developed ALL

An association of a viral infection in utero and development of acute lymphoblastic leukemia (ALL) has been suggested. Cytomegalovirus (CMV) has been reported as a leading agent of intrauterine infections resulting in some cases of congenital infections. The authors investigated the presence of prenatal CMV infection in children who later developed ALL. Guthrie cards were obtained from 48 children with ALL and 46 healthy children and were analyzed for the presence of CMV DNA by a real-time TaqMan PCR. CMV DNA was not detected in Guthrie cards from the children with ALL, from the control healthy children. The results show that prenatal CMV infection does not seem to be associated with later development of childhood ALL.     

Häufigkeit der konnatalen Zytomegalie in der Bundesrepublik Deutschland

Introduction. Cytomegalovirus (CMV) is the leading cause of congenital infection. 90–95% of infected infants are free of symptoms at birth and 5–10% are suffering from symptomatic disease. Methods. Between 1.11.1997 and 31.10.1999 clinical, laboratory and demographic data were monthly collected from standardized case reports. A congenital CMV infection was documented by isolation of virus, antigen or DNA in the first or second week of life and serologically. Results. There were 65 infants with congenital symptomatic CMV disease and 32 infants with presumtive congenital CMV disease. 45 out of 97 children were foreigners. 34 patients were treated with ganciclovir. In 13 of them the indication for virostatic treatment did not seem to be correct. Conclusion. The prevalence rate of congenital CMV infection in Germany is about 2/1000 infants. A virostatic therapy should be initiated in children with symptomatic CMV disease within the first 2 weeks of life.     

CMV seroconversion in pregnants and the incidence of congenital CMV infection

In this study, it was aimed to determine the ratio of CMV seroconversion in pregnant women, the prevalence of maternal CMV infection and also the incidence of congenital CMV infection in their newborns in the Antalya region of Turkey. During a one-year period, CMV-specific IgG and IgM were determined in all (n: 1027) pregnant women admitted at 8 to 20 weeks of gestation, an according to the presence or absence of anti CMV-IgM and CMV-IgG, pregnant women were classified as seropositive, seronegative and having maternal CMV infection. Differentiation of primary and recurrent CMV infection in women with both CMV-IgM (+) and CMV-IgG (+) antibody was determined by the avidity index (AI) of anti-CMV IgG. Ultrasonographic examination was done and amniocentesis was performed at 21 to 23 weeks of gestation in pregnants with primary infection. CMV DNA was investigated in the amniotic fluid by quantitative polymerase chain reaction (qPCR). Pregnants with recurrent infection were followed only by ultrasonography for the presence of fetal abnormalities. Neonates born to mothers with CMV infection were examined for the findings of congenital CMV infection and screened for anti- CMV-IgM, CMV DNA and CMV antigenemia in the first two weeks of life. The rate of seropositivity was found as 98.5% and the rate of seronegativity as 1.5% in pregnant women. The prevalence of maternal CMV infection was found as 1.2% and among these pregnant women, the incidence of primary and recurrent maternal CMV infection was 0.3% (3 women) and 0.8% (12 women), respectively. Congenital CMV infection was detected in one of the newborns born to mothers with primary infection while no infection was detected in any of the newborns of mothers with recurrent CMV infection, so the incidence of congenital CMV infection was found as 0.1% and the rate of intrauterine infection following the primary maternal infection was 33%. In conclusion, seroprevalence rate of CMV in pregnants is high and most (66%) infections are recurrent maternal CMV infection in our region. Thus, it does not seem to be cost-effective to screen all pregnant women for CMV infection, as in the other countries with high seropositivity rate.     

Prevalence and clinical aspects of congenital cytomegalovirus infection

OBJECTIVES: The objectives of the present study were to determine the prevalence of congenital CMV infection, as well as to evaluate the importance of this agent as cause of congenital disease, and to describe the clinical manifestations in children attended at a General Hospital in Ribeir?o Preto, SP, Brazil. POPULATION AND METHODS: A first group including 189 newborns and their mothers was evaluated for the prevalence of the congenital CMV infection. A second group including 130 newborns and 74 infants who presented clinical manifestations of congenital disease were also investigated to evaluate the importance of the CMV as a cause of this disease and to describe the clinical findings. Diagnosis of congenital CMV infection was established by detecting the virus using viral isolation in tissue culture, polymerase chain reaction DNA amplification in urine samples and detection of specific anti-CMV IgM and IgG by immunofluorescence indirect test. RESULTS: The prevalence of congenital CMV infection was 2.6% and the prevalence of CMV antibodies in mothers was 95%. In the first group, none of the 5 congenitally infected presented clinical apparent disease at birth, although one of them had intracranial calcifications. In the second group, CMV was recognized as a causative of congenital disease in 12 children (5.9%). Of these, 10(83%) were identified after the neonatal period. The clinical findings included hepatosplenomegaly (75%), jaundice with direct hyperbilirubinemia (42%), neurologic disease consisting of microcephaly and intracranial calcifications in 42% of these children. CONCLUSIONS: The prevalence of congenital CMV infection was similar to that reported in other studies about highly immune populations. Infants with asymptomatic congenital CMV infection may have diseases of the central nervous system that are not clinically evident at birth, such as punctate calcifications. CMV infected patients who are symptomatic at birth have a multisystem disease, and the differential diagnosis of any newborn with clinical abnormalities including involvement of the hepatobiliary, hematopoietic and central nervous systems should include congenital CMV infection. CMV was an important agent of these abnormalities, and the majority of symptomatic patients were identified after the neonatal period, making the diagnosis more difficult.     

Congenital cytomegalovirus infection - a common cause of hearing loss of unknown aetiology

Aim: The aim of this study was to investigate the role of congenital cytomegalovirus (CMV) infection as a cause of various types of sensorineural hearing loss (SNHL) in a group of nonsyndromic children with otherwise unknown aetiology of hearing loss. Furthermore, the occurrence of combined congenital CMV infection and connexin 26 (Cx26) mutations was investigated. Methods: The dried blood spot (DBS) cards of 45 children with various degrees of hearing deficits and 46 children with severe/profound hearing loss were tested for CMV DNA with polymerase chain reaction (PCR) technique. The DBS cards of the 46 children with severe/profound hearing loss were also analysed for Cx26 mutations. Results: Of the 45 children with various degrees of hearing loss, nine were positive for CMV DNA (20%). The nine children represented severe/profound, mild and unilateral hearing loss. From the 46 children with severe/profound hearing loss, nine of 46 (20%) were positive for CMV DNA. In addition, three of the CMV DNA‐positive children were carriers of mutations of Cx26. Conclusion: Congenital CMV infection is a high risk factor in hearing impairment among children.     

Congenital cytomegalovirus infection in twin pregnancies: viral load in the amniotic fluid and pregnancy outcome

Human cytomegalovirus (CMV) is the most common cause of viral intrauterine infection and fetal damage largely attributable to maternal primary infection. Most cases of congenital CMV infection in twins reported in the literature involved only 1 twin. We assessed the validity of polymerase chain reaction (PCR) and quantitative PCR on amniotic fluid (AF), at 21 to 22 weeks' gestation and at least 6 to 8 weeks after seroconversion, to predict the outcome of newborns in twin pregnancies. Two pregnant women with twin pregnancies and 1 woman with a triple pregnancy with primary CMV infection defined by the presence of immunoglobulin (Ig) M and low IgG avidity and/or by the presence of clinical symptoms and abnormal liver enzyme values were evaluated. CMV infection was found in 6 fetuses/newborns, 3 of whom were symptomatic. In the first twin pregnancy with diamniotic-dichorionic separate placentas, CMV symptomatic infection of the female twin was demonstrated by positive virus isolation and high viral load in AF. The male fetus was not infected as demonstrated by negative CMV culture and DNA detection in AF. In the triple pregnancy, the woman had a placenta with 2 monozygotic twins (females) and a separate placenta with a heterozygotic twin (male). The quantitative PCR results were 10(3) genome equivalents (GE)/mL of females AF and 1.9 x 10(5) GE/mL of male AF. Both female twins were asymptomatic at birth, whereas the male presented petechiae, thrombocytopenia, and cerebral ventriculomegaly. In the last twin pregnancy with fused dichorionic placentas, congenital CMV infection of both twins was diagnosed at birth in contrast with prenatal diagnosis. At time of amniocentesis, the left side twin was not infected as shown by negative results of CMV culture and DNA detection in the AF. CMV infection of the right side twin was demonstrated by positive CMV DNA detection with a CMV DNA load of 4.9 x 10(4) GE/mL and positive virus isolation in the AF. The morphologic and histologic examinations of the placentas strongly supported a prenatal horizontal acquisition of CMV infection. These twin pregnancies showed a marked difference in the quantity of virus load documented by the prenatal diagnosis suggesting that twin fetuses may react differently to primary maternal infection despite being exposed to the same maternal influences. A high viral load is correlated with congenital CMV infections symptomatic at birth. In such cases, with fetal infection of only 1 twin (at amniocentesis) and fusion of placentas, fetal outcome of both twins needs to be evaluated for the possibility of viral transfer from one fetus to the other.     

Urine polymerase chain reaction as a screening tool for the detection of congenital cytomegalovirus infection

OBJECTIVES: To define the incidence of congenital cytomegalovirus (CMV) infection in a defined population in Israel as diagnosed by urine polymerase chain reaction (PCR), and to assess the utility of this method for screening for congenital CMV infection. DESIGN: A convenient sample of urine specimens from asymptomatic newborns were subjected to CMV PCR. Positive results were validated by urine tube culture and by determination of serum CMV IgM antibodies. Maternal CMV IgG was determined in a representative sample of mothers. Newborns with positive urine specimens underwent full clinical evaluation. Epidemiological characteristics of the mothers were extracted from the medical records. SETTINGS: Two medical centres in Israel with different population characteristics. PATIENTS: A total of 2000 newborns (1000 in each medical centre). MAIN OUTCOME MEASURE: Presence of CMV DNA in the urine. RESULTS: Despite significant epidemiological differences between the populations in the two hospitals, the CMV seroprevalence was similar, 80.5% and 85%. Fourteen of the 2000 newborns screened (0.7%) were PCR positive. Urine culture was positive in nine of 10 specimens; IgM was positive in only two of 13 newborns with positive PCR. Eleven newborns underwent full or partial evaluation, and only one (9%) was symptomatic. CONCLUSIONS: The incidence of congenital CMV infection in the study population was 0.7%; over 90% were asymptomatic. Urinary CMV PCR is a reliable, rapid, and convenient method, and thus may serve as a screening tool for the detection of congenital CMV infection.     

婴儿先天性巨结肠与巨细胞病毒感染

为了解婴儿先天性巨结肠（ＨＤ）与巨细胞病毒（ＣＭＶ）感染的关系，对１９例２～１８个月的ＨＤ患儿（经病理证实）的血清、尿和组织块用病毒分离和ＤＮＡ探针杂交方法进行ＣＭＶ检测。结果：１９例ＨＤ患儿分离ＣＭＶ的１９份尿标本中２份污染，在１７份尿标本中７份阳性，阳性率为４１．２％；正常儿尿标本阳性率为１４．４％（Ｐ＜０．０５）。１９例ＨＤ血清中，ＣＭＶＩｇＭ抗体２例阳性，阳性率为１０．５％；正常儿阳性率为８．０％（Ｐ＞０．０５）。１９例ＨＤ痉挛段组织块中无一例ＣＭＶ阳性，但６例ＨＤ痉挛段组织块ＣＭＶ－ＤＮＡ探针杂交全部阳性，其中２例强阳性，阳性率为１００％。说明婴儿ＨＤ与ＣＭＶ感染关系密切，ＣＭＶ感染可能是包括ＨＤ在内的一些先天性畸形的重要致畸因素。     

Birth characteristics and growth pattern in children with congenital cytomegalovirus infection

Birth characteristics and growth pattern in 76 children with congenital cytomegalovirus (CMV) infection were compared to Swedish reference data. Infection classification was based on maternal sera during pregnancy. In 31 children the infection was primary and 31 children had reactivated (recurrent or secondary) congenital CMV infection. Infection type could not be determined in 14 children. Transient neonatal symptoms were apparent in 22 children and eight children had classical neurological CMV sequelae. Heterogeneous neurological disorders were found in 13 children. No significant differences in height, weight, and growth were found. The median follow-up time was 10 years. From 4 years old children with congenital CMV infection were taller than the reference standard. At 1 and 2 years, those children with primary congenital CMV infection were borderline shorter than reference standard, and from 4 years children with reactivated CMV infection were taller than the reference standard. In conclusion, no evidence was found verifying that congenital CMV infection causes short stature.