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Benign Familial Neonatal Seizures (BFNS) occur in normal newborns without perinatal neurological damage or metabolic abnormalities in the setting of a positive family history for neonatal seizures. This autosomal dominant disorder has an excellent prognosis, in contrast to most other causes of neonatal convulsions. This paper points out the need to include BFNS in the differential diagnosis of neonatal seizures and to specifically seek a family history to avoid an unnecessarily extensive diagnostic evaluation and poor prognostication. We present a family with one atypical and three classic cases. Further study of BFNS may reveal more definitive basic science information leading to the inclusion of variant forms into the currently narrow clinical definition.

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Mycoplasma hominis or Ureaplasma urealyticum have previously been isolated from cerebrospinal fluid (CSF) in 13 of 100 newborn infants tested from a high risk university hospital population where the mothers were of predominantly lower income and socioeconomic status and had often received little or no prenatal care. We sought to determine whether such infections occur in neonates born to women cared for mainly through private obstetric practices and who delivered in 4 suburban community hospitals. CSF cultures were done in 318 infants during an 8-month period. M. hominis was isolated from 9 and U. urealyticum from 5 CSF cultures. Four infants infected with U. urealyticum and 3 infected with M. hominis were born at term. One infant infected with U. urealyticum had a birth weight of less than 1000 g. In 5 infants clearance of the infecting organism was documented without specific treatment. Twelve infants had good perinatal outcomes regardless of treatment and 2 died. One death in a 2240-g infant infected with M. hominis was associated with Haemophilus influenzae sepsis and pneumonia. The other death occurred 3 days after birth in a 630-g infant infected with U. urealyticum who had evidence of meningitis and intraventricular hemorrhage. Results of this study suggest that mycoplasmas are common causes of neonatal CSF infections, not only in high risk populations, but also in the general population.

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The risk of acquiring cytomegalovirus (CMV) from infected infants concerns pediatric health-care workers, particularly those who may be pregnant. We determined the prevalence of CMV antibody, and thus of past infection, in groups of medical students and house staff, nurses, and physicians, and in groups of pregnant and nonpregnant young women in the community. Although age, sex, and race influenced the results, occupation did not. We then estimated the exposure of the health-care workers by determining the prevalence of CMV infection in three groups of asymptomatic infants for whom they provided care; CMV was shed in urine or saliva of 1.6 per cent of newborns, 13 per cent of premature infants hospitalized for over a month, and 5 per cent of older infants seen in outpatient settings. When we determined the incidence of primary infection in the adult groups by retesting the seronegative members about two years later, we found that the annual attack rates in the medical students (0.6 per cent), house staff (2.7 per cent), and nurses (3.3 per cent) were not higher than in young women in the community (2.5 per cent during pregnancy and 5.5 per cent between pregnancies). We conclude that although pediatric health-care workers frequently and unknowingly care for infants shedding CMV, this occupational contact confers no greater risk than that faced by young women in the community at large.

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A Chilean population was compared to low-income and middle/upper-class populations in Birmingham, Ala., with regard to prevalence of congenital cytomegalovirus infection as well as the importance of this infection in neonatal deaths. In the highly seroimmune Chilean (98%) and low-income Birmingham (82%) groups, congenital infections occurred more often (1.7% and 1.9%, respectively) than in the less immune (56%) middle/upper-income group in Birmingham (0.6%). In 407 autopsies reviewed in Chile no neonatal deaths were attributed to cytomegalic inclusion disease, whereas in Birmingham cytomegalovirus was the cause of death in nine of 938 (1%) newborn infants. These findings further support the concept that, despite an apparent lack of protection against intrauterine transmission, maternal immunity reduces the risk of severe fetal infection.

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Shedding of cytomegalovirus (CMV) was studied in 142 women who gave birth to congenitally infected infants and in 81 seropositive control mothers (mothers of uninfected infants). Viral cultures from the throat, vagina, and urine were obtained at intervals between one month and nearly 12 years after delivery. In both groups the prevalence of excretion of CMV was greater in younger women and fell to low levels by age 30. Considering all of the sites of infection, 60% of the mothers of infected infants were shedding CMV within the first three months post partum compared with 18% of the control mothers; CMV shedding rates declined during the first 12 months post partum to 35% in the former group and to 3% in the latter. More than three years after delivery, seven (15%) of 45 mothers who transmitted CMV still had viruria. The excretion of CMV is common and persistent in mothers of children with congenital infections due to CMV.

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We studied the incidence of primary and recurrent cytomegalovirus infection in 3712 pregnant women--2698 of middle to high income and 1014 of low income--to determine whether there were differences in the effects on the fetus. In the higher-income group, 1203 women (45 per cent) did not have antibodies to cytomegalovirus and were therefore susceptible to primary infection, as compared with 179 women (18 per cent) of low income. Congenital infection occurred more often (1.6 vs. 0.6 per cent) in infants in the low-income group. In this group it was associated with recurrent maternal infection more often (in 82 per cent) than with primary maternal infection, whereas in the upper-income group, it was associated with primary maternal infection in half the cases. Altogether, there were 32 cases of congenital cytomegalovirus infection - 16 in each group. Whereas primary maternal infection resulted in fetal infection in only half the cases, it was more likely to ge associated with clinically apparent disease than was recurrent infection. When these cases were combined with 28 cases of congenital infection retrospectively identified at other prenatal clinics, five of 33 infected infants born after primary maternal infection had clinically apparent disease, as compared with none of 27 born after recurrent maternal infection. We conclude that congenital cytomegalovirus infection resulting from primary maternal infection is more likely to be serious than that resulting from recurrent infection, and is more likely to occur in upper socioeconomic groups.

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Emergence of a multiply drug resistant Enterobacter cloacae during a seven-week period in 1980 caused amikacin to become the aminoglycoside of choice in the initial management of suspected sepsis in a neonatal intensive care unit. Recommended doses (7.5-10 mg/kg loading; 15 mg/kg in two divided doses IV) were given to 5 infants < or = 1,000 gm and to 13 larger babies. Trough levels 11.5 hours after a dose were 16.6 +/- 11.9 microg/ml in infants < or = 1,000 gm and 6.5 +/- 4.3 microg/ml in the larger infants (P < 0.02). Peak levels one hour postinfusion exceeded 40 microg/ml in 3 of 5 < or = 1,000-gm babies and 4 of 12 > 1,000-gm infants (P = NS). Overall, 7 of 10 peak and/or trough levels in < or = 1,000-gm infants were in the range considered toxic in adults, versus 7 of 24 in larger babies (P = 0.03). These data show that surprisingly excessive blood levels of amikacin are likely in infants < or = 1,000 gm and may also occur in larger infants using currently recommended dosage schedules. These unexpected findings emphasize the need to monitor drug levels and individualize therapy in very low birthweight infants.

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Cell-mediated immune responses in 27 infants and children with cytomegalovirus (CMV) infection acquired between birth and 1 year of age were compared with responses in 13 children who had neonatal herpes simplex virus (HSV) infection. Infection was asymptomatic in 25 of 27 CMV-infected children; the 13 patients with HSV infection were all ill as newborns. The median age when studied was 46 months for children infected with CMV and 24 months for those infected with HSV. We measured lymphocyte transformation responses (LTRs) to CMV antigens in the former group and to HSV type 1 (HSV-1) (and in six cases to HSV-2) in the latter group, with the results expressed as a stimulation index. Based on the results in seropositive and seronegative adult control subjects, stimulation indexes of greater than or equal to 3 were considered indicative of a positive LTR. Among the CMV-infected children, a positive LTR was observed in 0 to 13 assays performed before 1 year of age, 3 of 8 assays performed between 1 and 4 years of age, and 9 of 15 assays performed over 4 years of age. In contrast, a positive LTR to HSV-1 was seen in 15 to 18 assays performed in children under 1 year of age and in 14 of 16 assays performed in survivors of neonatal HSV infection older than 1 year. Six HSV-2-infected patients were tested simultaneously 13 times with HSV-1 and HSV-2 antigens. Those patients under 6 months of age responded similarly to each antigen, whereas those who were older had significantly higher LTRs to HSV-2. Children with CMV infection that was acquired early had persistently diminished specific LTRs. In contrast, after neonatal HSV infection, LTRs to HSV were present even in infancy and became more specific for the infecting type with increasing age.

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