4 9 4 Editorial correspondence The Journal of Pediatrics September 1993

intrauterine growth retardation frequently have arterial blood lac- tate concentrations in the range of 1.5 to 4.5 mmol/L. 3

Kevin H. Molteni, MD Assistant Professor of Pediatrics Section of Pediatric Nephrology

Medical College of Wisconsin Milwaukee, WI 53226

9/35/48603

REFERENCES

1. Relman AS. Metabolic consequences of acid-base disorders. Kidney Int 1972;1:347-59.

2. Harrington JT, Cohen JJ. Metabolic acidosis. In: Kassirer JP, Cohen J J, eds. Acid/base. Boston: Little, Brown, 1982:141.

3. Marconi AM, Cetin I, Ferrazzi E, Ferrari MM, Pardi G, Battaglia FC. Lactate metabolism in normal and growth- retarded human fetuses. Pediatr Res 1990;28:652-6.

Reply To the Editor:

We thank Dr. Molteni for his insight into this complicated med- ical problem. 1 However, the statistical analysis of choice for this population is analysis of variance repeated-measures design and subsequent Bonferroni-corrected two-tailed Student t test. 2 There- fore we found that the sepsis group had statistically significant plasma lactate elevations at every time point (p <0.003). Similarly, pH was not significantly different for the sepsis group with time. Thus alkalosis as a theoretical cause of elevation in plasma lactate is interesting but in this clinical setting is unlikely. A more impor- tant cause of the group's prolonged elevated plasma lactate concentration is an alteration in gluconeogenesisJ, 3 Although a larger sample size controlling pH, partial pressure of carbon diox- ide, and concentration of bicarbonate was suggested in a clinical setting, we pursued the mechanism in this complex clinical prob- lem by the use of an animal model 4 and the isolated perfused liv- er. 5 Finally, cord blood lactate concentration was pointed out to be lower in normal infants than in infants with intrauterine growth retardation. 6 We also believe that this is important. Precisely for this reason, our patients are matched for gestational age and are not growth retarded, and no samples contain cord blood.

Michael Fitzgerald, MD Masakatsu Goto, MD

Thomas F. Myers, MD W. Patrick Zeller, MD

Department of Pediatrics Loyola University Medical Center

Maywood, 1L 60153 9/35/48951

REFERENCES

1. Fitzgerald M J, Goto M, Myers TF, Zeller WP. Early meta- bolic effects of sepsis in the preterm infant: lactic acidosis and increased glucose requirement. J PEDIATR 1992; 121:951-5.

2. Hoel PG. Analysis of variance. In: Bradley RA, Hunger JS,

Kendall DG, Watson GS, eds. Elementary statistics. (Wiley Series in Probability and Mathematical Statistics.) New York: John Wiley & Sons, 1967:262-3.

3. Krebs HA, Woods HF, Alberti KGMM. Hyperlactataemia and lactic acidosis. Essays Biochem 1965;1:81-103.

4. Zeller WP, Goto M, Witek-Janusek L, Hurley RM. Mortal- ity, temporal substrate and insulin responses to endotoxic shock in zero, ten and twenty-eight day old rats. Surg Gynecol Obstet 191;173:375-83.

5. Goto M, Zeller WP, Pieken MP, Goto MP, Hurley RM. Li- popolysaccharide (LPS) alters suckling rat liver glycogenoly- sis. Circ Shock 1993;40:58-60.

6. Marconi AM, Cetin I, Ferrazzi E, Ferrari MM, Pardi G, Battaglia FC. Lactate metabolism in normal and growth-re- tarded human fetuses. Pediatr Res 1990;28:652-6.

Group B streptococcus serotype V*

To the Editor." We read with interest the article by Rench and Baker I in a re-

cent issue of THE JOURNAL. Their report details the first two cases of invasive neonatal group B streptococcal (GBS) disease known to be caused by type V, a new serotype of GBS.2 We have recently seen five patients with type V GBS, three with positive blood culture re- suits and two with positive results on surface culture. One patient with baeteremia was born at the Naval Hospital, San Diego, Ca- lif., and the remaining four patients were born at Wilford Hall Medical Center, San Antonio, Tex.

Three infants had clinical sepsis with bacteremia, one infant had clinical sepsis without documented bacteremia, and one infant had asymptomatic colonization. These preliminary observations do not support the emergence of a new, distinct clinical pattern of infec- tion with type V GBS but, instead, mimic the wide variability of symptoms produced by other GBS serotypes. All our patients with invasive GBS sepsis were discharged in good condition with no ap- parent sequelae.

The mothers of two of the three patients with bacteremia had been treated with antibiotics within 2 hours of delivery for chori- oamnionitis. The fact that the blood culture results were positive de- spite intrapartum antibiotics may reflect the virulence of this new se- rotype. However, the failure of intrapartum administration of antibi- otics to prevent bacteremia in neonates has been reported previously. 3

The two cases of type V GBS bacteremia that occurred at the primary study center (Wilford Hall Medical Center) were among nine patients with GBS bacteremia born during the 15-month study period (January 1992 to March 1993). There were 2048 total births at this institution during the study period, for an incidence of GBS

*The views expressed in this letter are those of the authors and do not reflect the official policy of the Department of Defense or other departments of the U.S. Government. The GBS serotyping was graciously performed by Dr. John A. Elliott and Dr. Richard Facklam at the Centers for Disease Control, Atlanta, Ga.