983 disaccharidase activity drops abruptly
20
at
weeks, presumably
when the fetus stops defxcating. Section de Génétique Médicale, Centre de Recherche Pédiatrique,
M. POTIER L. DALLAIRE S. B. MELANÇON
Hôpital Sainte-Justine, Montréal H3T 1C5, Québec, Canada
GROUP-B STREPTOCOCCI AT A LONDON HOSPITAL
SIR,—Group-B streptococci have emerged as important pathogens in the newborn. We have looked through the records to see if there has been a general increase in prevalence in this hospital or an increase among obstetric and neonatal patients. All haemolytic streptococci isolated from any site and all streptococci, whether haemolytic or not, when isolated in pure culture from a site normally sterile (e.g., blood and urine) have been identified by Lancefield grouping for many years. Computer-produced statistics are available from 1972, with a gap in
strains are included whether there was evidence of infection or not. There is no evidence for increasing prevalence. If the species had increased in virulence one might have expected an apparent increase in prevalence due, for example, to increased infection of the throat or urinary tract leading to increased investigation. During the past few years group-B streptococcal infection has been the commonest bacterial cause of death in the neonatal unit. The most likely reason for increased pathogenicity in neonates is, we think, the increased efficiency of rescue procedures resulting in a larger number of small premature babies who are especially at risk. All strains isolated from neonates in this hospital have been sensitive to penicillin. We therefore think that treatment of the mother directly membranes rupture or labour begins (whichever is the earlier) followed by treatment of the baby after delivery is indicated for all small premature babies. Group-B streptococcus is sometimes isolated from the umbilicus or ear of older neonates-which is not surprising since the organism is the most common hxmolytic streptococcus found in the vagina-but these babies come to no harm. We have no evidence of cross-infection with this species in our neonatal wards but no doubt such infection could happen as it does with other potential pathogens.
group-B
E. J. STOKES S. MEHTAR*
University College Hospital, London WC1 * Present address: don N1.
Department
of
Microbiology, Whittington Hospital,
Lon-
DARK-BROWN AMNIOTIC FLUID
SIR,-Dark-brown amniotic fluid is occasionally found at diagnostic amniocentesis done early in the second trimester. My colleagues and I have commented brieflyl on the possible significance of this, and I now present details of our observations.
Fig.1-Group-B streptococci as % of total isolates.
Fig. 2--,Group-B streptococci isolated stetric patients. 1974 when
some
records
were
from neonatal and ob
lost due
to
computer
change-
over.
The number of strains isolated monthly (repeats from the patient not included) in each year calculated from May to the end of April were as follows: 1972-73 highest number 20, lowest 7; in 1975-76 highest 31, lowest 10; and in 1976-77 highest 34, lowest 12. Fig. 1 shows the prevalence expressed as a percentage of all positive cultures. Fig. 2 shows the prevalence as a percentage of all isolates found in specimens received from the obstetric and neonatal wards. All same
Twenty-six patients were studied who, at amniocentesis at 14-20 weeks’ gestation, gave amniotic-fluid samples which were very dark brown in colour and which also often contained a fine, whitish sediment. One sample contained a trace of fresh red blood-cells. Sixteen of these fluids, including the one with the fresh red blood-cells, had alpha-fetoprotein (A.F.P.) values which were normal for the gestation. The mean value was 21 ug/ml. Ten fluids had very high A.F.P. values, the mean being 430 µg/ml. The sixteen patients with normal A.F.P. values were delivered of apparently healthy, singleton infants, within the normal weight range, at, or around, term. The ten with the raised A.F.P. levels all aborted severely macerated fetuses, 1½ 7 weeks after the amniocentesis. None of these fetuses had any congenital abnormality, but they were at an earlier stage of development than expected from their alleged gestational age. The dark-brown colour of the amniotic fluid is presumably due to old haemoglobin derived from an intra-amniotic haemorrhage some time before amniocentesis. It seems, however, that this finding should cause concern for the wellbeing of the fetus only if it is associated with a very high A.F.P level, these two observations signifying that the fetus is dying or dead. This information has been of use to the obstetricians in assessing the condition of the fetus. More recently, the last three patients in this group also underwent routine ultrasonography before amniocentesis. In each case no fetal heart beat could be detected. By contrast, the 29 cases of living fetuses with open neuraltube defects I have examined have never been associated with amniotic fluids of this colour. The liquor of anencephalics is usually red, being stained with fresh red blood-cells, presum1.
Blunt, S., Berry, A. C., Seller, M. J., Vaughan Williams, C. A. J. med. Genet. 1977, 14, 232.
20
at
weeks, presumably
when the fetus stops defxcating. Section de Génétique Médicale, Centre de Recherche Pédiatrique,
M. POTIER L. DALLAIRE S. B. MELANÇON
Hôpital Sainte-Justine, Montréal H3T 1C5, Québec, Canada
GROUP-B STREPTOCOCCI AT A LONDON HOSPITAL
SIR,—Group-B streptococci have emerged as important pathogens in the newborn. We have looked through the records to see if there has been a general increase in prevalence in this hospital or an increase among obstetric and neonatal patients. All haemolytic streptococci isolated from any site and all streptococci, whether haemolytic or not, when isolated in pure culture from a site normally sterile (e.g., blood and urine) have been identified by Lancefield grouping for many years. Computer-produced statistics are available from 1972, with a gap in
strains are included whether there was evidence of infection or not. There is no evidence for increasing prevalence. If the species had increased in virulence one might have expected an apparent increase in prevalence due, for example, to increased infection of the throat or urinary tract leading to increased investigation. During the past few years group-B streptococcal infection has been the commonest bacterial cause of death in the neonatal unit. The most likely reason for increased pathogenicity in neonates is, we think, the increased efficiency of rescue procedures resulting in a larger number of small premature babies who are especially at risk. All strains isolated from neonates in this hospital have been sensitive to penicillin. We therefore think that treatment of the mother directly membranes rupture or labour begins (whichever is the earlier) followed by treatment of the baby after delivery is indicated for all small premature babies. Group-B streptococcus is sometimes isolated from the umbilicus or ear of older neonates-which is not surprising since the organism is the most common hxmolytic streptococcus found in the vagina-but these babies come to no harm. We have no evidence of cross-infection with this species in our neonatal wards but no doubt such infection could happen as it does with other potential pathogens.
group-B
E. J. STOKES S. MEHTAR*
University College Hospital, London WC1 * Present address: don N1.
Department
of
Microbiology, Whittington Hospital,
Lon-
DARK-BROWN AMNIOTIC FLUID
SIR,-Dark-brown amniotic fluid is occasionally found at diagnostic amniocentesis done early in the second trimester. My colleagues and I have commented brieflyl on the possible significance of this, and I now present details of our observations.
Fig.1-Group-B streptococci as % of total isolates.
Fig. 2--,Group-B streptococci isolated stetric patients. 1974 when
some
records
were
from neonatal and ob
lost due
to
computer
change-
over.
The number of strains isolated monthly (repeats from the patient not included) in each year calculated from May to the end of April were as follows: 1972-73 highest number 20, lowest 7; in 1975-76 highest 31, lowest 10; and in 1976-77 highest 34, lowest 12. Fig. 1 shows the prevalence expressed as a percentage of all positive cultures. Fig. 2 shows the prevalence as a percentage of all isolates found in specimens received from the obstetric and neonatal wards. All same
Twenty-six patients were studied who, at amniocentesis at 14-20 weeks’ gestation, gave amniotic-fluid samples which were very dark brown in colour and which also often contained a fine, whitish sediment. One sample contained a trace of fresh red blood-cells. Sixteen of these fluids, including the one with the fresh red blood-cells, had alpha-fetoprotein (A.F.P.) values which were normal for the gestation. The mean value was 21 ug/ml. Ten fluids had very high A.F.P. values, the mean being 430 µg/ml. The sixteen patients with normal A.F.P. values were delivered of apparently healthy, singleton infants, within the normal weight range, at, or around, term. The ten with the raised A.F.P. levels all aborted severely macerated fetuses, 1½ 7 weeks after the amniocentesis. None of these fetuses had any congenital abnormality, but they were at an earlier stage of development than expected from their alleged gestational age. The dark-brown colour of the amniotic fluid is presumably due to old haemoglobin derived from an intra-amniotic haemorrhage some time before amniocentesis. It seems, however, that this finding should cause concern for the wellbeing of the fetus only if it is associated with a very high A.F.P level, these two observations signifying that the fetus is dying or dead. This information has been of use to the obstetricians in assessing the condition of the fetus. More recently, the last three patients in this group also underwent routine ultrasonography before amniocentesis. In each case no fetal heart beat could be detected. By contrast, the 29 cases of living fetuses with open neuraltube defects I have examined have never been associated with amniotic fluids of this colour. The liquor of anencephalics is usually red, being stained with fresh red blood-cells, presum1.
Blunt, S., Berry, A. C., Seller, M. J., Vaughan Williams, C. A. J. med. Genet. 1977, 14, 232.
