1053 SEROTYPES, MORTALITY,
PHOSPHOLIPID COMPOSITION OF TRACHEAL ASPIRATES OF INFANTS WITH EARLY-ONSET GROUP-B STREPTOCOCCAL
AND AGE DISTRIBUTION IN SALMONELLA
MENINGITIS CASES
SEPSIS
*Results as % of
cal
phospholipid phosphorus.
picture resembling
R.D.S.
if infected with
group-B strepto-
cocci, but that the respiratory distress is not due to a deficiency or to an
alteration in surfactant
Rather, the respiratory distress
phospholipid composition.
to interference with surfactant function by bacterial products or tissue exudate, or to mechanical obstruction of alveoli with exudate.
*Available antisera insufficient for accurate identification.
given parenterally.
Salmonellee were isolated from C.S.F. alone and blood in 9, C.S.F. and stool in 5, and c.s.F., blood, and stool in 8. Organisms probably gained entry into the c.s.F. by haematogenous spread from primary infection in the gastrointestinal tract. in 29 cases,
c.s.F.
Departments of Microbiology and Pædiatrics, University of Natal Medical School, Durban, South Africa
La Jolla, California 92093, U.S.A.
Southwest Neonatal Center, Sunrise Hospital, Las Vegas, Nevada
BRIAN S. SAUNDERS T. ALLEN MERRITT
ELSA KIRKPATRICK LOUIS GLUCK
BERNARD H. FELDMAN
NECROTISING ENTEROCOLITIS P. C. APPELBAUM
J. SCRAGG
GROUP-B STREPTOCOCCI IN THE NEWBORN
SIR,-You refer (March 5, p. 520) to the striking clinical resemblance of early-onset group-B streptococcal infection in the newborn to the respiratory-distress syndrome (R.D.S.). Hyaline membranes are a prominent finding at necropsy in both conditions, and in cases of group-B sepsis streptococci have been demonstrated in the membranes.1 Although similar clinically and radiographically, the two syndromes show marked differences when pulmonary surfactant is examined. R.D.S. is the clinical expression of surfactant deficiency, and infants with R.D.S. have a deficiency of surfactant and an immature phospholipid pattern in tracheal effluent.2,3 In R.D.S. lecithin has less palmitic acid esterified to the beta carbon and phosphatidyl glycerol is absent.2 Three full-term infants with clinical symptoms similar to R.D.S. and culture-confirmed group-B sepsis were studied in our laboratory. Phospholipid composition of tracheal aspirates shows a mature pattern when separated by two-dimensional
thin-layer chromatography (table). Gas-liquid chromatography on the acetone-precipitable lecithin demonstrated that 69% of the beta carbon fatty acids were palmitic acid (mature pattern). The results suggest that early-onset group-B streptococcal sepsis does not alter the phospholipid pattern of pulmonary surfactant in full-term infants. The clinical counterpart of this is the finding by Ablow et al. that, for mechanical ventilations of patients with group-B streptococcal pneumonia, lower distending pressures are needed than in infants with R.D.S.4 We conclude that a full-term infant can present with a clini1. 2.
Department of Pediatrics, University of California, San Diego
may be due
Katzenstein, A. L., Davis, C., Braude, A. J. infect. Dis. 1976, 133, 430. Hallman, M., Feldman, B. H., Kirkpatrick, E., Gluck, L. Pediat. Res. (in the press). 3. Obladen, M., Merritt, T. A., Gluck, L. ibid. (in the press). 4. Ablow, R. C. and others New Engl J. Med. 1976, 294, 65.
SIR,-In your editorial (Feb. 26, p. 459) the most significant part for us was towards the end where you discuss the evidence that a major xtiological factor in necrotising enterocolitis (N.E.C.) is infection of the bowel wall with gram-negative organisms such as Klebsiella. This is important because these organisms are not available to produce infection in the gut of the breast-fed baby. The bacterial population is almost exclusively made up of bifidobacteria under these circumstances. It would thus be expected that, as has been proven in rats, breast milk would protect against N.E.C. More evidence of a direct type is needed. Breast milk has been used exclusively for lowbirthweight babies in the Children’s Hospital in Helsinki since the 1920s, and Dr N. Hallman tells us that N.E.C. is very rare there. There are some parallels between N.E.c. and the "pig-bel" of the New Guinea highlands. Both seen to be related to the bacterial flora in the intestinal canal-in N.E.C. with a dominance of gram-negative organisms and in pig-bel with clostridia. Division of Population, Family and International Health School of Public Health,
University of California, Los Angeles, California, 90024, USA
DERRICK B. JELLIFFE E. F. PATRICE JELLIFFE
BLOOD-LEAD AND MENTAL RETARDATION
SIR,-While prospective studies relating lead concentrations in blood obtained by heelprick to subsequent mental performance’ would seem a form of investigation free from bias, we will shortly2 be reporting on a very strong association between placental lead level and fetal and neonatal death; this leads us to believe that the concentration of lead in the placenta may often be secondary to disturbances in placental function associated with lethal fetal disease. 1. Moore, M. R., Meredith, P. A., Goldberg, A. Lancet, 1977, i, 717. 2. Wibberley, D. G., Khera, A. K., Edwards, J. H., Rushton, D. I. J. med. Genet. (in the press).
PHOSPHOLIPID COMPOSITION OF TRACHEAL ASPIRATES OF INFANTS WITH EARLY-ONSET GROUP-B STREPTOCOCCAL
AND AGE DISTRIBUTION IN SALMONELLA
MENINGITIS CASES
SEPSIS
*Results as % of
cal
phospholipid phosphorus.
picture resembling
R.D.S.
if infected with
group-B strepto-
cocci, but that the respiratory distress is not due to a deficiency or to an
alteration in surfactant
Rather, the respiratory distress
phospholipid composition.
to interference with surfactant function by bacterial products or tissue exudate, or to mechanical obstruction of alveoli with exudate.
*Available antisera insufficient for accurate identification.
given parenterally.
Salmonellee were isolated from C.S.F. alone and blood in 9, C.S.F. and stool in 5, and c.s.F., blood, and stool in 8. Organisms probably gained entry into the c.s.F. by haematogenous spread from primary infection in the gastrointestinal tract. in 29 cases,
c.s.F.
Departments of Microbiology and Pædiatrics, University of Natal Medical School, Durban, South Africa
La Jolla, California 92093, U.S.A.
Southwest Neonatal Center, Sunrise Hospital, Las Vegas, Nevada
BRIAN S. SAUNDERS T. ALLEN MERRITT
ELSA KIRKPATRICK LOUIS GLUCK
BERNARD H. FELDMAN
NECROTISING ENTEROCOLITIS P. C. APPELBAUM
J. SCRAGG
GROUP-B STREPTOCOCCI IN THE NEWBORN
SIR,-You refer (March 5, p. 520) to the striking clinical resemblance of early-onset group-B streptococcal infection in the newborn to the respiratory-distress syndrome (R.D.S.). Hyaline membranes are a prominent finding at necropsy in both conditions, and in cases of group-B sepsis streptococci have been demonstrated in the membranes.1 Although similar clinically and radiographically, the two syndromes show marked differences when pulmonary surfactant is examined. R.D.S. is the clinical expression of surfactant deficiency, and infants with R.D.S. have a deficiency of surfactant and an immature phospholipid pattern in tracheal effluent.2,3 In R.D.S. lecithin has less palmitic acid esterified to the beta carbon and phosphatidyl glycerol is absent.2 Three full-term infants with clinical symptoms similar to R.D.S. and culture-confirmed group-B sepsis were studied in our laboratory. Phospholipid composition of tracheal aspirates shows a mature pattern when separated by two-dimensional
thin-layer chromatography (table). Gas-liquid chromatography on the acetone-precipitable lecithin demonstrated that 69% of the beta carbon fatty acids were palmitic acid (mature pattern). The results suggest that early-onset group-B streptococcal sepsis does not alter the phospholipid pattern of pulmonary surfactant in full-term infants. The clinical counterpart of this is the finding by Ablow et al. that, for mechanical ventilations of patients with group-B streptococcal pneumonia, lower distending pressures are needed than in infants with R.D.S.4 We conclude that a full-term infant can present with a clini1. 2.
Department of Pediatrics, University of California, San Diego
may be due
Katzenstein, A. L., Davis, C., Braude, A. J. infect. Dis. 1976, 133, 430. Hallman, M., Feldman, B. H., Kirkpatrick, E., Gluck, L. Pediat. Res. (in the press). 3. Obladen, M., Merritt, T. A., Gluck, L. ibid. (in the press). 4. Ablow, R. C. and others New Engl J. Med. 1976, 294, 65.
SIR,-In your editorial (Feb. 26, p. 459) the most significant part for us was towards the end where you discuss the evidence that a major xtiological factor in necrotising enterocolitis (N.E.C.) is infection of the bowel wall with gram-negative organisms such as Klebsiella. This is important because these organisms are not available to produce infection in the gut of the breast-fed baby. The bacterial population is almost exclusively made up of bifidobacteria under these circumstances. It would thus be expected that, as has been proven in rats, breast milk would protect against N.E.C. More evidence of a direct type is needed. Breast milk has been used exclusively for lowbirthweight babies in the Children’s Hospital in Helsinki since the 1920s, and Dr N. Hallman tells us that N.E.C. is very rare there. There are some parallels between N.E.c. and the "pig-bel" of the New Guinea highlands. Both seen to be related to the bacterial flora in the intestinal canal-in N.E.C. with a dominance of gram-negative organisms and in pig-bel with clostridia. Division of Population, Family and International Health School of Public Health,
University of California, Los Angeles, California, 90024, USA
DERRICK B. JELLIFFE E. F. PATRICE JELLIFFE
BLOOD-LEAD AND MENTAL RETARDATION
SIR,-While prospective studies relating lead concentrations in blood obtained by heelprick to subsequent mental performance’ would seem a form of investigation free from bias, we will shortly2 be reporting on a very strong association between placental lead level and fetal and neonatal death; this leads us to believe that the concentration of lead in the placenta may often be secondary to disturbances in placental function associated with lethal fetal disease. 1. Moore, M. R., Meredith, P. A., Goldberg, A. Lancet, 1977, i, 717. 2. Wibberley, D. G., Khera, A. K., Edwards, J. H., Rushton, D. I. J. med. Genet. (in the press).
