Prevention of neonatal group B streptococcal infection

Author: Chris Keenan
Date: June, 1998

Group B streptococci (including Streptococcus agalactiae) are the leading bacterial causes of neonatal illness and death, causing invasive disease in 1.8 infants per 1,000 live births.[1,2] These bacteria asymptomatically colonize the vaginal or rectal areas of 10 to 30 percent of pregnant women.[1] In these women, group B streptococci may cause preterm labor or membrane rupture, as well as urinary tract infections, chorioamnionitis, postpartum endometritis, postpartum wound infection, septic pelvic thrombophlebitis, endocarditis and sepsis.[3,4] Clinically diagnosed maternal intrapartum infection is strongly associated with five-minute Apgar scores below 6, neonatal seizures and unexplained spastic cerebral palsy in infants of normal birth weight.[5] Up to 2 percent of maternal carriers deliver infants with invasive group B streptococcal disease, most of which is caused by inutero infection.[1]

Between 30 and 70 percent of infants born to mothers with group B streptococcal colonization also become colonized at rectal, umbilical or oral sites, but only a small proportion of these infants develop sepsis.[6] Early-onset disease, usually manifested as sepsis or pneumonia, is diagnosed in the first six days of life and accounts for approximately 80 percent of neonatal group B streptococcal infections.[1] Late-onset disease is identified at seven or more days of life and is usually neonatal sepsis or meningitis.

The results of a population-based surveillance system indicate that the mortality rate for neonatal group B streptococcal infections is less than 10 percent, primarily because of prompt treatment of infected infants.[3] Based on data from early case series, long-term neurologic sequelae have been estimated to occur in up to 30 percent of meningitis survivors.[1] The Centers for Disease Control and Prevention (CDC) has been conducting group B streptococcal disease surveillance in three urban areas across the country, as well as in the entire state of Maryland.[7] From 1993 through 1995, the overall annual incidence of early-onset group B streptococcal disease in the surveillance areas declined 24 percent, from 1.7 cases per 1,000 live births in 1993 to 1.3 cases per 1,000 live births in 1995.

Identification of Group B Streptococci

The CDC has described methods for culturing group B streptococci (Table 1).[1] Identification takes 24 to 48 hours. Although a selective medium is considered essential for the culture, a recent survey[8] indicated that fewer than 10 percent of hospital-based microbiology laboratories use an appropriate medium. A transport medium is acceptable, but cultures performed with this medium may fail to identify 10 percent of colonized women.[9]

TABLE 1 Method for Culturing Group B Streptococci from Pregnant Women

1. Without using a speculum, sweep a single swab over the skin from the vaginal introitus to the anus.

2. Place the swab in a suitable transport medium such as Amies medium; the swab may remain in this medium for up to four days.

3. Inoculate the swab in one of the following selective broth media:

a. Todd-Hewitt broth supplemented with nalidixic acid (15 g per mL) and either colistin (10 g per mL) or gentamicin (8 g per mL). or

b. A commercially available culture medium such as SBM or Lim broth.

4. Incubate the culture for 18 to 24 hours.

5. Subculture the broth culture to a sheep-blood agar plate and incubate for 18 to 24 hours.

6. Inspect and identify organisms suggestive of group.13 streptococci:

a. For definitive identification, use group B streptococcal antigen detection methods.

b. For presumptive identification, use the CAMP (Christie, Atkins and Munch-Petersen) test.

Adapted from Centers for Disease Control and Prevention. Prevention of perinatal group B streptococcal disease: a public health perspective. MMWR Morb Mortal Wkly Rep 1996;45(RR-7):1-24 [Published erratum appears in MMWR Morb Mortal Wkly Rep 1996;45(31):679].

Anogenital cultures obtained six or more weeks before delivery show poor concordance with results obtained at the time of delivery. Therefore, antenatal cultures after 34 weeks of estimated gestation are recommended.[10]

Rapid diagnostic tests for group B streptococci are specific, but sensitivity is variable and sometimes unacceptably low.[11] With a reported sensitivity and specificity of 95 percent and 99.5 percent, respectively, the AccuProbe group B streptococcal test (manufactured by GenProbe) is a possible exception.[12] Confirmation of this level of performance is necessary in additional studies.

Rapid tests perform better in heavily colonized women than in women who are lightly colonized. However, many infected infants are born to lightly colonized women.

Strategies for Preventing Group B Streptococcal Disease

The four strategies for preventing perinatally acquired group B streptococcal disease are eradication of colonization during pregnancy, postnatal chemoprophylaxis of infants with intramuscularly administered penicillin, vaginal antisepsis with topical chlorhexidine gluconate (Hibiclens) and systemic intrapartum chemoprophylaxis.

Of these approaches, eradication of colonization during pregnancy is ineffective.[3] In contrast, postnatal chemoprophylaxis of infants using a single dose of intramuscularly administered penicillin was effective in one large, randomized, controlled trial.[3] In this trial, the incidence of invasive group B streptococcal infection was reduced by 65 percent. However, a prospective, randomized study[1] of this strategy in low-birth-weight infants failed to show a difference in morbidity or mortality related to group B streptococcal infection between the intervention and the control groups.

In the third strategy, an effort is made to eliminate group B streptococci during labor. A randomized, controlled, double-blinded study[3] of vaginal antisepsis with topical chlorhexidine was conducted in Sweden, but the trial was too small to show any effect on the prevention of neonatal group B streptococcal disease. Consequently, this strategy is not recommended at the present time.

Systemic intrapartum chemoprophylaxis appears to be the most effective means of preventing group B streptococcal disease in neonates. A nonrandomized trial[13] involving more than 30,000 Australian women sought to obtain universal antepartum screening cultures and provide universal intrapartum chemoprophylaxis for all carriers of group B streptococcal. Although the study had numerous limitations (e.g., delivery before a prenatal culture was obtained, failure to obtain a prenatal culture and failure to administer antibiotics during labor), the neonatal group B streptococcal infection rate was 0.5 cases per 1,000 live births in the screened women compared with one case per 1,000 live births in the control group.

A review[14] of the intrapartum chemoprophylaxis of perinatal group B streptococcal infections identified four randomized, controlled trials of adequate methodologic integrity that had been published as of December 1992.[15-18] However, no study was noted to be of particularly good quality. Three studies showed a statistically significant reduction in infant colonization; the other study did not consider this outcome. Three trials failed to show a statistically significant reduction in proven or probable group B streptococcal infection, although a promising trend was noted; the other study did not consider this outcome.

While the authors of the review[14] expressed concerns about the appropriateness of using these studies in a meta-analysis, other investigators[19] have used them anyway and have suggested that intrapartum chemoprophylaxis results in a 30-fold reduction of early-onset group B streptococcal disease. Despite the limitations of studies supporting the efficacy of intrapartum chemoprophylaxis, the preponderance of evidence to date indicates that such treatment is effective in preventing early-onset group B streptococcal disease.

Public Health Dilemmas

Preventing neonatal group B streptococcal disease requires identifying high-risk infants before they are born while simultaneously minimizing the iatrogenic risk posed to uninfected infants. Thus, the challenge facing prenatal care providers (and the authoritative professional bodies to which they turn for guidance) is the correct identification of high-risk pregnant women.

Universal Screening

The first method for preventing neonatal group B streptococcal disease is universal screening of pregnant women, either antepartum or peripartum (at the time of parturition or rupture of the membranes). As discussed earlier in this article, current diagnostic technology is not sufficiently reliable to permit rapid, accurate peripartum identification of colonized women. However, properly obtained and processed antepartum cultures correctly identify most women who are colonized at the time of labor.

Treatment Based on Risk Factors

[23.] Rouse DJ, Goldenberg RL, Cliver SP, Cutter GR, Mennemeyer ST, Fargason CA Jr. Strategies for the prevention of early-onset neonatal group B streptococcal sepsis: a decision analysis. Obstet Gynecol 1994;83:483-94.

[24.] Mohle-Boetani JC, Schuchat A, Plikaytis BID, Smith JD, Broome CV. Comparison of prevention strategies for neonatal group B streptococcal infection, A population-based economic analysis. JAMA 1993;270:1442-8.

[25.] Yancey MK, Duff P. An analysis of the cost-effectiveness of selected protocols for the prevention of neonatal group 8 streptococcal infection. Obstet Gynecol 1994;83:367-71.

[26.] Gotoff SP, Boyer KM. Prevention of early-onset neonatal group B streptococcal disease. Pediatrics 1997;99:866-9.

[27.] Fargason CA Jr, Peralta-Carcelen M, Rouse DJ, Cutter GR, Goldenberg RL. The pediatric costs of strategies for minimizing the risk of early-onset group B streptococcal disease. Obstet Gynecol 1997;90:347-52.

[28.] Agnoli FL. Group B streptococcus: perinatal considerations. J Fam Pract 1994;39:171-7.

CHRIS KEENAN, M.D., M.P.H., practices family medicine at Clinica Campesina Family Health Services, Lafayette, Colo. He is also assistant professor in the Department of Family Medicine at the University of Colorado School of Medicine, Denver, and associate residency director of the Clinica Campesina track of the University Hospital's family medicine residency program in Denver. Dr. Keenan attended medical school at the University of Missouri, Columbia. He completed family practice and general preventive medicine residencies at the University of Massachusetts Medical Center Worcester, where he also earned a master's degree in public health.

Address correspondence to Chris Keenan, M.D., Clinica Campesina Family Health Services, 1345 Plaza Court North, Unit 1A, Lafayette, CO 80026. Reprints are not available from the author.

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