Intrauterine diagnosis of cytomegalovirus and rubella infections by amniocentesis.

OBJECTIVE: To establish a correlation between the presence of cytomegalovirus (CMV) or rubella virus in amniotic fluid obtained through amniocentesis and fetal infection. DESIGN: Case series. SETTING: Five hospitals in the Montreal region. Virology testing was done at the Virology Research Centre, Institut Armand-Frappier, Laval, Que. PATIENTS: Thirteen pregnant women infected with CMV, 3 with rubella, their 15 babies and 2 fetuses. Twelve of the women with CMV infection were recruited from a prospective study of CMV infection in pregnancy. Infection in the other women was detected through routine laboratory diagnostic testing. INTERVENTION: Amniotic fluid samples were cultured for CMV and rubella virus. Congenital infection of the neonates was established through isolation of either virus from pharyngeal mucus and urine specimens collected during the first 3 days of life or from fetal tissue if the pregnancy was terminated. MAIN RESULTS: CMV was cultured from the amniotic fluid of three of the CMV-infected women and from the pharyngeal mucus and urine specimens of their infants. Of the three women with rubella the amniotic fluid of one (who had a twin pregnancy) was positive for rubella virus. After the in-utero death of one fetus she underwent a therapeutic abortion of both. Examination of fetal tissue indicated that both fetuses had been infected with rubella virus. Each of the two other women with rubella gave birth to an uninfected, healthy infant. CONCLUSIONS: We found a strong correlation between the isolation of CMV or rubella virus from the amniotic fluid and the presence of congenital infection. This suggests that amniocentesis used to detect the presence of a virus is a useful method for the diagnosis of fetal infection.

Changing pattern of neonatal streptococcal septicemia.

In recent years viridans streptococcus has emerged as a new and significant cause of neonatal septicemia. This article reports our experience over a 6-year period with respect to the prevalence and clinical presentation of viridans streptococcal vis-à-vis Group B streptococcal septicemia in neonates. Viridans streptococcus was the organism most frequently isolated taking into account all positive blood cultures for streptococci in newborns. Although some similarities were observed between the two groups, viridans streptococcal septicemia was associated with a later onset of symptoms and with a lower incidence of respiratory distress and leukopenia. Clinical findings suggest that viridans streptococcus is a less virulent organism than is Group B streptococcus. The viridans streptococcus should be considered a pathogen in the sick neonate.

Sacrococcygeal tumour in infancy.

A newborn infant delivered after 33 1/2 weeks' gestation was operated on for sacrococcygeal teratoma. This tumour contained an unusual intra-abdominal cystic component that caused pulmonary problems. Amniography and echography were useful for diagnosing this lesion in utero.

Neuraminidase in cultured fibroblasts and leucocytes of homozygotes and heterozygotes for the mucolipidosis II gene (I-cell disease).

The significance of neuraminidase deficiency reported to be the primary defect in mucolipidosis II has been evaluated by determination of this enzyme activity in cultured fibroblasts, culture medium, and leucocytes from homozygote and heterozygous carriers of the disease. A new and sensitive fluorometric assay of neuraminidase was used with sodium (4-methylumbeliferyl-alpha-D-N-acetylneuraminate) as substrate. We report: 1) nearly total deficiency of neuraminidase in mucolipidosis fibroblasts, 2) partial deficiency of this enzyme in leucocytes of one patient, 3) this decreased activity ceases to exist following Triton X-100 treatment, and 4) intermediary mean neuraminidase activity in fibroblasts and leucocytes from obligate heterozygotes. Although these results would be consistent with the suggestion that neuraminidase deficiency is the primary defect in this disease, evidence from the work of other authors suggests that the enzyme deficiency results from a secondary effect of the mucolipidosis II mutation.