Selective Intrapartum Chemoprophylaxis of Neonatal Group B Streptococcal Early-Onset Disease. III. Interruption of Mother-to-Infant Transmission

Boyer, Kenneth M.; Gadzala, Cecile A.; Kelly, Peggy D.; Gotoff, Samuel P.

doi:10.1093/infdis/148.5.810

Cited by 242 publications

(72 citation statements)

References 22 publications

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“…Many investigations have addressed this and clearly established an increased risk of EOS after 18 h of ROM. [14][15][16] Acquisition of EOS is also associated with a number of other well-described factors that, if present, would support the need to consider observation or evaluation of the newborn for infection. These include a maternal fever >38 1C, chorioamnionitis, prolonged or preterm ROM, poor prenatal care, poor maternal nutrition, a history of recurrent abortion, low birth weight, maternal substance abuse, difficulty in delivery, birth asphyxia and meconium staining.…”

Section: Early Versus Late Infectionsmentioning

confidence: 99%

The changing spectrum of neonatal infectious disease

Plano

2010

J Perinatol

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To understand the changing spectrum of neonatal infectious disease, one must first be familiar with the history, the variety of organisms and the progression of change of neonatal infections over the years. As progressively more immature neonates are surviving, the spectrum of infectious disease has changed in response to current medical practice responsible for this success and to selective pressures on the microorganisms. The surviving very low birth weight infants are at a significant risk for contracting infections from this expanding repertoire of pathogens. Microorganisms once thought seemingly benign and nonpathogenic are now commonly accepted as pathogens and are among the most likely organisms to cause infections in this extremely vulnerable patient population. When considering the possible identity of infecting organisms and attempting to tailor specific therapies to decrease unwanted consequences, one must consider the level of maturity and the age of neonate, as well as the intensity of care necessary for a successful outcome. This brief review focuses primarily on the changing spectrum of bacterial and fungal infections and will not substantially address viral infections.

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Section: Early Versus Late Infectionsmentioning

confidence: 99%

The changing spectrum of neonatal infectious disease

Plano

2010

J Perinatol

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“…Several years after the demonstration of the efficacy of intrapartum antibiotic prophylaxis, the American Academy of Pediatrics and the American College of Obstetricians and Gynecologists both embraced the concept but issued different clinical guidelines in 1992. [1][2][3][4][5] The resultant controversy and implementation difficulties led the Centers for Disease Control and Prevention (CDC) to orchestrate the development of consensus guidelines in 1996 that were embraced by multiple organizations devoted to improving perinatal care. [6][7][8][9][10][11][12][13][14] These guidelines advocated the use of either screening for maternal group B streptococcal rectovaginal colonization or clinical risk factors to determine the need for intrapartum prophylaxis.…”

Section: Introductionmentioning

confidence: 99%

Neonatal Early-onset Group B Streptococcal Disease in the Era of Intrapartum Chemoprophylaxis: Residual Problems

et al. 2003

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OBJECTIVE:To identify limitations of current strategies for intrapartum prophylaxis of neonatal early-onset group B streptococcal infection. METHODS:Retrospective review of infants with culture-proven early-onset group B streptococcal infection admitted to two nurseries and their mothers from July 1992, when ACOG and AAP guidelines for intrapartum prophylaxis were first issued, through December 2001. Information was recorded regarding clinical risk factors for early-onset group B streptococcal infection, collection and processing of specimens to assess maternal colonization, delivery of prophylaxis, duration of hospitalization before delivery, and outcome. RESULTS:Among 92 infants with early-onset group B streptococcal infection admitted from 23 institutions, 68 had received no intrapartum prophylaxis. Of these 68 who received no prophylaxis, 34 had identifiable risk factors before delivery (32 clinical, two positive maternal culture), while 34 had no risk factors. Prenatal culture for group B streptococcal colonization was performed in 22 of these women. Of the 18 cultures that were negative for group B streptococcus, 15 were obtained using suboptimal culture technique or were collected more than 6 weeks before delivery. Of the 68 with no prophylaxis, 14 required extracorporeal membrane oxygenation and three died. Of the 24 who received some intrapartum prophylaxis, nine had received Ztwo doses for Z4 hours immediately before delivery. Among the 24 receiving some intrapartum prophylaxis, two required extracorporeal membrane oxygenation and one died. No deaths occurred in those who received >4 hours of prophylaxis, although one such infant required extracorporeal membrane oxygenation. After the CDC guidelines were issued in May 1996, there was a decrease both in the number of cases of early-onset group B streptococcal infection (56 versus 36) as well as in the number with clinical risk factors but no intrapartum prophylaxis (24/56 (43%) versus 5/28 (18%)). CONCLUSIONS:The use of clinical risk factors alone will inevitably result in missed opportunity for intrapartum antibiotic prophylaxis. With maternal screening, false-negative results will be reduced but not necessarily eliminated by assuring that specimens are obtained from proper sites using selective media within 6 weeks of delivery. Better strategies are needed to assure timely administration when prophylaxis is indicated. The nine neonates with early-onset group B streptococcal infection despite intrapartum antibiotics for the recommended duration illustrate that disease may occur even when guidelines are implemented appropriately.

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“…Several culture-based studies have reported higher carriage rates of GBS in the rectum than in the vagina [18,26,27], supporting the idea that the gastrointestinal tract is the reservoir for vaginal GBS. Meyn et al [28] showed that rectal colonization with GBS was the most significant predictor of vaginal colonization, suggesting that the vagina becomes colonized with GBS as a result of transfer of the organism from the rectum to the vagina.…”

Section: Introductionmentioning

confidence: 89%