Natural History of Neonatal Colonization With Group B Streptococci

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Natural

History

of Neonatal

Colonization

With

Group

B Streptococci

William T. Speck, M.D., John M. Driscoll, M.D., Richard A. Polin, M.D.,

and Herbert S. Rosenkranz, Ph.D.

From the Departinent of Pediatrics, College of Plitjsieian.x and Surgeons, Columbia 1.iiit’ersitij. .\‘eu’ York, and the Department of Microbiology, New York Medical College, Valhalla

ABSTRACT. Thirteen percent of the newborns in our study group were colonized with group B streptococci on day 3. This colonization rate appeared constant during the first two weeks of life and then decreased to 5%. Of the babies colonized on day 3, 59% and 91% were culture-negative on days 14 and 42, respectively. Sixty-five percent of the babies carrying group B streptococci on day 14 acquired this microorganism following discharge (day 3). Babies colonized with staphylococci or Escherichia coli were found to have

decreased probability of colonization with group B strepto-cocci. Pediatrics 60:356-359, 1977, GROUP B STREPTOCOCCI, NEONATAL COLONIZATION, BACTERIAL INTERFERENCE.

factors responsible for neonatal colonization with this microorganism. As part of a study to deter-mine the effect of antiseptic cord care on bacte-rial colonization in the newborn, we studied group B streptococcal colonization in our newborn population.5 In the present report we

characterize the evolution of group B

strepto-coccal colonization in these neonates and describe the existence of bacterial antagonism between this microorganism and other bacteria

which normally colonize the newborn infant.

MATERIALS AND METHODS

Serious consideration of the factors underlying bacterial colonization of the newborn infant began 30 years ago when nursery epidemics of staphylococcal pyoderma appeared in significant numbers. During the next 20 years it was estab-lished that other, equally virulent, microorga-nisms, both Gram-positive and Gram-negative, were also capable of causing epidemic disease in newborn infants. However, the importance of the group B Streptococcus as a significant cause of disease in newborn infants was established only during the past decade. The reasons for the emergence of this group of organisms as etiolog-ical agents of neonatal disease remain unclear. Attempts to control neonatal streptococcal disease have thus far been unsuccessful. Such attempts have included antibiotic treatment of asymptomatic maternal and neonatal carriers, as well as changing the nature of routine newborn cord care.i The establishment of alternative and more effective therapeutic approaches has been hampered by a lack of information on all of the

Infants born to mothers attending the routine

antenatal clinic of the Sloane Hospital for

Women (Columbia-Presbyterian Medical Center) were eligible for admission to the study. All study

infants were born between September 1, 1974,

and July 31, 1975. The study subjects were all

healthy newborns. A child was excluded from

consideration for any of the following reasons: (1)

the infant’s mother was considered by the

obstet-rical staff to be a high-risk patient in whom complications during gestation, labor, or delivery

were likely to develop; (2) a maternal

complica-tion developed during gestation, labor, or

Received December 6, 1976; revision accepted for publica-tion March 3, 1977.

Supported in part by a grant-in-aid from Marion Laborato-ries, Kansas City, Missouri.

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COLONIZATION RATES OF NEWBORN INFANTS BY GROUP

B /3-HEMOLYTIC STREPTOCOCCI AND BY OTHER

MICROOlI(;ANISMS

INTERFERENCE BETWEEN GROUP B STREPTOCOCCI ANI) OTHER MIcRooRGANISMS

RESULTS

TABLE I TABLE II

ARTICLES

357

.‘%fi(’roorganisni Day % of’

Infants

Total No.

of Babies Cultured

Group B streptococci 3

14 42 13 14 5 268 251 223

S. wrcus 3

14 35 67

268 251

S.(‘pi(lerflhi(li,S’ 3

14 43 63

268 251

E. (‘eli 3

14 22 28

268 251

delivery or the mother received antimicrobial agents during the last trimester of her pregnancy;

(

3) the infant was born following cesarean section;

(4) complications developed in the infant during

labor or delivery; and (5) illness of any sort was diagnosed or suspected in the infant during the period of hospitalization. All study infants were housed in one of four nurseries located on three floors of the same hospital. Two hundred sixty-eight neonates were included in the study. The nasopharynx and umbilicus of the infants were cultured on days 3, 14, and 42 of life and processed by standard bacteriological procedures. All isolates of group B streptococci were identi-fled by routine methods and confirmed by sero-logic testing with group-specific antisera. For the present analysis, an infant is reported as culture-positive if one of the culture sites (or both) yields

group B Streptococcus. Data related to bacterial

antagonism deal only with the microbiological findings of the site from which the group B

Streptococcus was recovered. If both culture sites yielded this microorganism, data from both sites are included.

The group B streptococcal colonization rate for

study infants at the time of hospital discharge (day 3) was 13% (Table I). The colonization rate appeared constant through the first two weeks of life, e.g., 14% on day 14; however, by day 42, the streptococcal colonization rate had decreased to 5% (Table I). Most of the infants colonized at the

time of hospital discharge (day 3) spontaneously

became culture-negative by day 14, e.g., 20 of the

34 infants (59%) colonized on day 3 were culture-negative on day 14 and 31 of these 34 infants (91%) were culture-negative by day 42. A large

Co-Colonizing Day Sites With Sites With

Microorganism Group B

Without Co-Colonizer

Group B Wit/i Co-Colonizer S.aureus 3 14 34 22 6 7

S.epidennkfts 3 29 12

E. coli 14 3 14 17 31 19 8 1() 6

number of study children became colonized with

group B streptococci following discharge from

the newborn nursery. Thus, 26 of the 40 infants

(

65%) colonized on day 14 were culture-negative at the time of hospital discharge (day 3). The source(s) of these non-hospital-acquired microor-ganisms was not identified in this study.

In the present study we were able to document bacterial antagonism between group B strepto-cocci and other microorganisms that normally colonize the skin of newborn infants. Thus, on day 3, out of 40 sites colonized by group B strepto-cocci only six (15%) were co-colonized with

Staphylococcus aureus (Table II), while the

remaining sites (85%) were colonized in the

absence of this microorganism. Similarly, for S.

epidermidis, 29% (12 of 41) of the sites containing

group B streptococci were also colonized with

this Staphylococcus while 71% (29 of 41) of the patients colonized with group B streptococci were devoid of S. epidermidis (Table II). Evidence for bacterial interference between staphylococci and the group B Streptococcus was still evident on

day 14 (Table II). The magnitude of this

antag-onism can better be appreciated when it is

realized that while the overall colonization rate with group B Streptococcus is quite low (e.g., 13% on day 3, Table I), the overall colonization rate with staphylococci is quite high (e.g., in excess of 35% and 60% on days 3 and 14, respectively, Table I). Hence, the bacterial interference reported in Table II is highly significant.

Antagonism between group B streptococci and

E.

coli was also observed (Table II). Thus on day 3, 76% (31 of 41) of sites colonized with group B streptococci were devoid of E. coli as compared to 24% (10 of 41) that were co-colonized with E. coil. This interference persisted for the first two weeks of life (Table II). Here again, a comparison of overall colonization rates with group B

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tococcus and E. coli reveals (Table I) that twice as many babies are colonized by the latter, which again indicates the interference between these microorganisms is significant.

The colonization rate by group B Streptococcus on day 14 appeared to be influenced by the previous colonization history. Thus, of 26 sites colonized on day 14, 22 (85%) were free of S.

aureus on day 3 while only 4 (15%) were cob-nized by this microorganism on day 3. Similarly,

of 23 sites colonized on day 14 by group B streptococci, only eight (35%) had a previous history of S. epidermidis colonization on day 3

while the remainder (65%) were not colonized by this microorganism.

DISCUSSION

The /3-hemolytic streptococci, which we now

designate group B, were initially described as

animal pathogens.6 Following Lancefield’s group-ing of $-hemolytic streptococci, the group B microorganisms were identified as normal

inhabi-tants of the genitourinary system.7 It was later

established that these microorganisms were capable of causing disease in human populations.8 In 1958 Nyhan and Fousek described a case of group B streptococcal meningitis in a newborn infant. The impact of group B streptococci in neonatal populations was first emphasized in

1964 by Eickoff and associates’#{176} who reported an increased frequency of group B streptococcal infections in newborn infants at the Boston City Hospital. Franciosi and his associates” in Denver and Baker and co-workers’2 in Houston reviewed

large series of neonatal group B streptococcal

infections and separated the neonatal disease into two clinical syndromes based on the age of onset. The “early onset” or “septicemic” type of infec-tion, presumably due to acquisition of this micro-organism at the time of labor or delivery, occurs within the first few days of life and is character-ized by fulminating septicemia and respiratory insufficiency. The case fatality rate often approaches 50%. The “delayed onset” or

“menin-gitic” streptococcal syndrome, due to nosocomial

acquisition of group B streptococci following delivery, is characterized by the appearance of signs and symptoms following the first week of life. This syndrome characteristically involves the central nervous system and has a lower mortality than the “early” disease.

The group B streptococcal colonization rate for study infants was 13% at the time of hospital discharge. It is conceivable that a higher recovery rate for this microorganism would have been obtained if enrichment culture techniques had

been utilized or more sites were routinely cultured.’3’5 Nevertheless, our neonatal group B

streptococcal colonization rate agrees with

previously published results, which have ranged from 3% to 26%.’”

A large number of study children became colonized with group B streptococci following discharge from the newborn nursery. The source of these microorganisms could not be ascertained in this study; however, it is conceivable that some of these late colonizers were positive at the time of discharge (day 3) and that the extent of

colonization was too low to be detected by the

procedures employed in this study. It is also

possible that these infants became colonized through contact with an infected nonhospital source. The observation that previously unde-tected group B streptococcal colonization occurs following hospital discharge is new and might explain recurrent group B streptococcal disease in newborn infants. Similarly, these observations

emphasize the difficulty in utilizing

hospital-derived cultures to identify infants “at risk” for

group B streptococcal disease.

The observation that most of the infants cob-nized at the time of hospital discharge sponta-neously became culture-negative has not been

reported previously. A possible explanation for

this phenomenon might be that organisms

consid-ered “normal flora” of the skin, i.e.,

staphvbo-cocci, are generally inhibited during the first few

weeks of life by “cord prophylaxis” with such

agents as triple dye, povidone-iodine, and bacitra-cm.3 ‘ Following discharge, the antibacterial

action of these agents declines, allowing the staphylococci to recolonize the infant. These latter microorganisms appear to inhibit the

growth of group B streptococci. Indeed in this

study an inverse correlation was found between

colonization with group B streptococci and both

S. epidermidis and S. aureus.

Antagonism between bacterial species was first

commented on by Roberts in 1874 when he

described “antagonism between the growth of

certain races of , In the present study we were able to document bacterial antagonism

between group B streptococci, staphylococci, and

K coil. The mechanisms responsible for the bacte-nab interference observed in this study have yet to be elucidated. These findings on bacterial antag-onism may partially explain the changing epide-miobogy of neonatal bacterial infections. The recent emergence of group B streptococci as a significant cause of neonatal septicemia may simply reflect new and improved methods for

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coloniza-ARTICLES

359

tion. Evidence in support of this possibility was obtained in the course of these studies when it

was found that infants receiving cord treatment that effectively eliminated staphylococci exhib-ited a significantly higher colonization rate with

group B streptococci than control babies.5 The

role of bacterial antagonism in controlling neonatal infection as well as providing informa-tion of the changing epidemiology of neonatal bacterial disease deserves further investigation.

REFERENCES

1. HaIl RT, Barnes W, Krishnan L, et al: Antibiotic treatment of parturient women colonized with group B streptococci. Am J Obstet Gynecol

124:630, 1976.

2. Steere AC, Aber RC, Warford LR, et al: Possible nosocomial transmission of group B streptococci in a newborn nursery. J Pediatr 87:784, 1975.

3. Paredes A, \‘ong P. Yow MD: Failure of penicillin to eradicate the carrier state of group B Streptococcus

in infants. J Pediatr 89:191, 1976.

4. Wald ER, Snyder NIT, Gutberles RL: Group B strepto-coccal colonization of newborns: Effect of triple dye cord care. Presented at the Fifteenth Inter-science Conference on Antimicrobial Agents and Chemotherapy, Washington, DC, September 1975.

5, Speck \VT, Driscoll JM, Polin RA, et al: Staphylococcal and streptococcal colonization of the newborn infant: Effect of antiseptic cord care. Pediatr Res 10:3.35, 1976.

6. Patterson MJ, Hafeez AEB: Group B streptococci in human disease. Bacteriol Rev 40:774, 1976. 7, Lancefield RC: A serological differentiation of human

and other groups of hemolytic streptococci. J Exp

Med 57:571, 1933.

8. Fry RM: Fatal infections by hemolytic Streptococcus

group B. Lancet 1:199, 1938.

9. Nyhan WL, Fousek MD: Septicemia of the newborn.

Pediatrics 22:268, 1958.

10. Eickoff TC, Klein JD, Daly AK, et al: Neonatal Sepsis and other infections due to group B beta hemolytic streptococci. N EngI J Med 271:1221, 1964.

1 1. Franciosi BA, Knostman JD, Zimmerman BA: Group B

streptococcal neonatal and infant infections. J Pediatr 82:707, 1973.

12. Baker CJ, Barrett FF, Gordon RC, Yow MD: Suppura-tive meningitis due to streptococci of Lancefield group B: A study of 33 infants. J Pediatr 82:724,

1973.

13. Baker CJ, Clark DJ, Barrett FF: Selective broth medium for isolation of group B streptococci. AppI Micro-biol 26:884, 1973.

14. Baker CJ, Clark DJ, Barrett FF: Erratum. Appl Micro-biol 27:817, 1974.

15. Badri MS, Zawaneh 5, Cruz A, et al: Rectal colonization with group B streptococci. Pediatr Res 10:394,

1976.

16. Yow MD: Epidemiology of group B streptococcal infec-tions, in Krugman S, Gershon AA (eds): Infections of the Fetus and the Newborn Infant. New York, Alan

R Liss mc, 1975, p 1959.

17. Pildes RS, Ramamurthy RS, Vidyasagar D: Effect of triple dye on staphylococcal colonization in the newborn infant. J Pediatr 82:987, 1973.

18. Anonymous: Antibiosis amongst skin microorganisms. Lancet 2: 1080, 1975.

ACKNOWLEDGMENT

We wish to thank Miss M. Brooks, Miss M. Housner, and

Mrs. Jane ONeill for their assistance and Mrs. M. Steiner for her assistance in preparation of the manuscript.

OUR KLEENEX CULTURE

. . . It takes about 850 acres of Canadian timber to print one Sunday’s New

York Times. . . . The New York Times sells for 50 (1972) and contains more

paper and typography than an unillustrated novel selling for $7.95. While the

Times carries about 500 photographs and drawings in its Sunday edition and a

novel does not, book-binding costs average 22 per book. It costs the city of New York nearly 10 per copy each week to clean up discarded copies of the Sunday New York Times.

Design for the Real World, 1973

Noted by R.J.H.

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1977;60;356

Pediatrics

William T. Speck, John M. Driscoll, Richard A. Polin and Herbert S. Rosenkranz