Continued Early Onset Group B Streptococcal Infections in the Era of Intrapartum Prophylaxis

L.S. Pulver; M.M. Hopfenbeck; P.C. Young; G.J. Stoddard; K. Korgenski; J. Daly; C.L. Byington

Disclosures

J Perinatol. 2009;29(1):20-25. 

In This Article

Discussion

We found an EOGBS infection rate of 0.42 per 1000 live births in the study population, a rate that is 75% higher than the national average of 0.24 per 1000 live births for Caucasian deliveries. We also found that the majority of the cases appeared to be associated with failure of microbiological screening despite adherence to the CDC recommendations. These higher than expected infection rates remained constant over the 4-year study period, even as the CDC's 2002 guidelines for universal GBS screening and targeted intrapartum prophylaxis became increasingly adopted and practiced in the IH system.[15]

The clinical findings in the cases of EOGBS described in our study were similar to those classically described.[16] Most occurred in term infants, presented with respiratory symptoms within 24 h of birth, and were associated with bacteremia with or without pneumonia.[17] Although term infants accounted for 42 of the 54 cases of EOGBS, all of the deaths occurred in preterm infants. This difference in mortality is consistent with other studies.[18,19]

The strategy for prevention of EOGBS contains two essential elements. First, all pregnant women are to be screened for the presence of GBS by the collection of rectovaginal swabs between 35 and 37 weeks' gestation, with the swabs then being processed according to CDC protocols. Second, women who are GBS positive are to receive appropriate IAP. We found that there were apparent breakdowns in both of these elements that may have led to the some of the cases of EOGBS and that some of these elements were, at least potentially, modifiable.

A total of 12 infants in this study were born prematurely, and therefore did not have GBS screening results available at the time of maternal presentation to labor and delivery. Prematurity is not a modifiable aspect of the current EOGBS prevention strategy, though it is an indication for antibiotic prophylaxis.

Failure to perform GBS screening in term pregnancies was not a significant problem. Of the women delivering term infants with EOGBS, 93% had prenatal screening for GBS. Two of the three women who were not screened were women who chose alternatives to traditional health care, delivered at home, and did not have prenatal care at a medical facility. If these two women are excluded from the analysis, then 98% of women who received prenatal care in a medical setting and delivered an infant with EOGBS were screened for GBS carriage. This high rate clearly demonstrates the acceptance of GBS screening by obstetrical providers in Utah.

Failure to administer appropriate IAP to mothers who were known to be GBS positive when they presented in labor was associated with seven cases of EOGBS disease. In one case, an infant was delivered at home, thereby eliminating IAP as recommended by CDC guidelines. In four cases, the interval between IAP administration and delivery was less than 4 h; the timing of antibiotic administration in relation to delivery of the infant is difficult to control and, in some instances, it may not be possible to administer antibiotics in the time frame suggested by CDC guidelines. Two of the GBS-positive women received clindamycin with no susceptibility testing, a necessary step in determining whether clindamycin will be adequate for prevention of EOGBS. Within the IH system in 2007, GBS isolates that underwent susceptibility testing had a 20% rate of clindamycin resistance. These findings underscore the importance of routine susceptibility testing when processing maternal GBS screening cultures in penicillin-allergic women. Although providers practicing in IH facilities have protocols in place to promote adherence to the CDC guidelines, it is possible that some of the failures to initiate timely and appropriate prophylaxis could be attributed to lack of adherence to the CDC prophylaxis recommendations. In addition, the fact that 31 term infants with negative maternal GBS screens developed EOGBS disease despite adherence to recommended screening and treatment guidelines should serve as a reminder to newborn care providers that the current strategy is not perfect.

Finally, the most common area of apparent breakdown in EOGBS prevention was the high rate of negative GBS screening cultures. Of the 39 women who had prenatal screening for GBS and delivered infants with EOGBS, 79% had a screening test performed at the appropriate time that was negative. A similar high rate of negative screening tests was reported by Puopolo et al.[20] who found that 82% of mothers who gave birth to term infants with EOGBS disease had negative GBS screens. There are several possible explanations for these negative screens. Some of the screening specimens may have been collected, transported or processed inappropriately. Numerous clinicians provided prenatal care to these women, and it is possible that some of them may have used improper technique when collecting the specimens. Although IH microbiological laboratories follow the guidelines for GBS culture processing detailed by the CDC, some of the screening cultures were processed at non-IH facilities that may not have followed the CDC guidelines. There was, however, no difference in the proportion of negative results in women whose babies developed EOGBS, and whose GBS screening had been performed outside the IH system, compared with those in whom it was performed in the IH system.

Negative prenatal GBS cultures could be due to maternal factors that affect the sensitivity of culture. Several maternal factors are known to affect GBS culture results, even when specimens are properly obtained and processed. For example, use of antibiotics and various intravaginal preparations are known to cause false-negative GBS screening cultures.[21] Likewise, GBS maternal colonization may have occurred late in pregnancy, after the prenatal screening test was performed.[22,23] However, we found that women undergoing GBS testing at the time of labor and delivery were just as likely to have false-negative GBS cultures as those undergoing prenatal screening between 35 and 37 weeks' gestation. This suggests that the cause of negative screening cultures is more likely due to problems associated with GBS culture collection or processing than the late gestational acquisition of GBS.

Our study suggests that current techniques for screening too often produce negative results in a substantial number of women whose babies develop EOGBS. A negative test may falsely reassure providers as they consider their treatment of mothers and infants. In addition, some infants will inevitably be delivered before the recommended screening time, and some women may acquire GBS after having been screened. Ascertainment of maternal GBS status during labor, using sensitive and rapid molecular techniques has the potential to overcome these problems. Rapid polymerase chain reaction (PCR) assays, using either conventional or fluorogenic techniques, have a sensitivity of 97% and a specificity of 100% compared with traditional culture results.[24] Turnaround time for these tests ranges from 30 to 45 min for the newer fluorogenic PCR assay to 100 min for conventional PCR assays.[24] Numerous commercial PCR assays are currently available with sensitivities and specificities approaching 100%.[25] The FDA has approved the use of a real-time PCR assay for detection of GBS DNA from combined vaginal and rectal swab specimens.[26] A cost-effectiveness analysis performed by Haberland et al.[27] found that use of rapid PCR to detect maternal GBS colonization at the time of labor saved money and resulted in decreased morbidity and mortality compared with risk-based approaches to neonatal GBS disease prevention. IH is moving toward implementation of this technology in all of its delivery facilities.

This study has several limitations: (1) we used a rigorous definition of EOGBS disease, that is, a positive culture. This may have resulted in an underestimate of the number of actual clinical cases. (2) The rates of EOGBS disease reflect experience in the IH system. Though it accounts for approximately 60% of births within Utah, IH may not accurately represent the experience of the rest of Utah's population. (3) Moreover, EOGBS disease in Utah may differ from the rest of the country due to genetic, environmental or geographic differences unique to Utah, and the reasons for continuing cases that we found may also differ. Previous studies have examined EOGBS disease in urban, racially diverse, or otherwise higher risk populations. This study is the first to report increased EOGBS cases in a predominantly low-risk setting with near universal prenatal screening in eligible patients, thus allowing the processes of prevention to be more closely examined.

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