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Fwd: GBS stuffFrom: DoctorJoe@aol.comMon May 13 08:24:38 1996
Just in case anyone was interested, here's the ACOG Technical Bulletin on Group B Strep from 1992. I picked it up from the new ACOG web page. If you want it, just save this letter (or selected parts of it). If you don't, just skip this message and don't waste your online time. Joe P. --------------------- Forwarded message: --------------------- Subj: GBS stuff --------------------- Date: 96-05-10 14:54:27 EDT From: DoctorJoe To: DoctorJoe ACOG Technical Bulletin Number 170 - July 1992 GROUP B STREPTOCOCCAL INFECTIONS IN PREGNANCY Group B streptococcus (GBS) (Streptococcus agalactiae) has been recognized as the leading cause of life-threatening perinatal infections in the United States. The spectrum of disease includes maternal chorio-amnionitis and endomyometritis, as well as neonatal sepsis, pneumonia, and meningitis (1, 2). Additionally, there is some evidence that colonization may be associated with an increased incidence of premature rupture of membranes and preterm delivery (3-5). While penicillin and ampicillin are effective for treating streptococcal infections in both mother and baby, improved protocols for timely diagnosis, early treatment, and prevention remain a clinical challenge. Epidemiology Approximately 15-40% of pregnant women are asymptomatic carriers of GBS (1, 6-8). Studies of the distribution of GBS by anatomic site have demonstrated that vaginal and rectal colonization is more common than colonization of the cervix or urinary tract (1, 3, 5-9). The rectum may be the depot site for chronic GBS carriage. The colonization rate shows both geographic and individual variability. For instance, vaginal cultures taken serially during pregnancy may be intermittently positive in the absence of specific therapy against GBS (6, 8). In the United States, approximately 12,000 proven neonatal GBS infections occur each year (1). Fifty percent of all perinatal GBS colonization is transmitted from mother to baby at parturition. Colonized infants may be born with or may develop early-onset (-7 days after birth) infections manifested by bacteremia, pneumonia, or meningitis. Of early-onset infections, two thirds are clinically apparent within 6 hours of birth. As a group, early-onset infections have a mortality rate of 15% or higher. While the overall attack rate (infection in colonized infants) for this form of early-onset neonatal sepsis due to GBS is only 1-3/1,000 live births, the attack rate is increased to 10/1,000 in babies born to mothers with perinatal vaginal colonization (1, 10-12). This attack rate increases to as high as 40/1,000 (1/25) if there are additional risk factors, such as prematurity, prolonged rupture of membranes, amniotic fluid colonization, maternal fever during labor, or an infected prior child (1, 10, 11, 13). When neonatal GBS infection occurs after the first few days of life, meningitis becomes a predominant part of the clinical syndrome. The overall attack rate for this late-onset neonatal infection is 0.5-1.0/1,000 live births. The route of transmission in late-onset infections may be from mother to infant intrapartum (approximately 50% of cases) or from nosocomial or community sources (1, 10). Manifestations of symptomatic maternal infection due to GBS include chorioamnionitis, endomyometritis, cystitis, and pyelonephritis (2, 5, 9-11, 13). One study reported the rate of postpartum fever to be 22% in women colonized during the second trimester and only 4% in controls (14). Another study reported the incidence of maternal puerperal infection due to GBS on a clinic service to be 13/1,000 deliveries; 95% of these infected patients were delivered by cesarean birth (2). Heavy colonization of the genitourinary tract increases the attack rate for both mothers and babies (15). Cesarean delivery appears to be a particularly prominent risk factor for postpartum endomyometritis (2, 16). Additional risk factors reported to have statistical significance include low serum antibody to the capsular antigens of GBS and maternal diabetes (1). Laboratory Tests Culture is the usual method for the diagnosis of GBS colonization (1). The isolation of GBS may be enhanced by the use of selective broth media that inhibit the growth of other microorganisms. Use of nonselective broth (routine transport medium) and plating onto a nonselective solid medium (eg, blood agar plates) diminishes the detection of GBS vaginal colonization by 50% or more (1). The only limitation of culture as a method is the time required for a result, making its use most practical antenatally. Rapid diagnostic tests based on direct identification of the group-specific polysaccharide antigen of GBS have been developed for commercial use (9, 17, 18). These tests use latex agglutination or enzyme-linked immunosorbent assay (ELISA) technology. In optimal circumstances, the result can be obtained in less than 1 hour from the time of specimen collection. Some of these tests may be suitable for use at the site of clinical care, rather than in a central laboratory. Rapid antigen tests may enhance clinical decision-making when a prompt decision is needed regarding antibiotics or delivery. However, the clinician should be aware that rapid tests will have both false-positive and false-negative results when compared with cultures. Antigen tests will outperform the Gram stain, which is not recommended for screening (7, 18). Both rapid antigen tests and culture methods can be adapted to provide a semiquantitative measurement of the degree of GBS colonization. It is generally accepted that the likelihood of symptomatic perinatal infection increases with increasing colonization and that both cultures and rapid antigen tests yield more accurate results in patients with high counts of GBS (9, 15). Screening Clinical studies have shown that screening for GBS in pregnant women may be done by testing the vagina or rectum (Table 1) as well as urine (5) and cervix (9). However, screening protocols for GBS have not been used widely enough to set a standard for routine obstetric care (19). Because the prevalence of GBS colonization of the lower urogenital tract is high (15-40%) and the attack rate among the infants of colonized mothers is low (1-2%) (11), chemoprophylaxis for all colonized women has not been perceived as either justifiably beneficial or cost-effective in the United States. The nature of GBS colonization of the genitourinary and lower intestinal tracts is such that no one site has shown to be exclusively predictive of perinatal infection. Over the course of pregnancy, a positive culture site may spontaneously become negative while a negative culture site spontaneously becomes positive. However, when antenatal lower vaginal and rectal cultures have been performed concurrently, their predictive value for maternal GBS colonization at delivery is 96% (11). When screening has been done, the patient should be informed of the result and of the factors that will require intrapartum antibiotic administration. The pediatrician should be informed of culture-positive antepartum patients who have had an uncomplicated delivery without antibiotic chemoprophylaxis. Chemoprophylaxis Various regimens of antibiotic chemoprophylaxis have been suggested for: 1) decreasing the frequency of early-onset neonatal colonization or infection, particularly when there has been premature labor or premature rupture of membranes, and 2) decreasing maternal puerperal infection (Table 1). Although antepartum treatment of the term pregnant woman and her sexual partner for asymptomatic vaginal colonization with GBS has been shown to decrease genital colonization (20), patients receiving antepartum antibiotics during the third trimester have a high rate of relapse (67%) by term if treatment is discontinued (6). On the other hand, it has been shown that a single course of antepartum treatment for GBS urinary tract colonization (a likely indicator of heavy genital colonization) with oral antibiotics may reduce the frequency of preterm labor and premature rupture of the membranes (5). Intrapartum intravenous antibiotics have been shown to prevent mother-to-baby transmission of GBS colonization and early-onset neonatal sepsis and also to decrease the rate of postcesarean endomyometritis (11, 12, 15, 21). Antibiotics used as chemoprophylaxis should be continued as treatment when there is ongoing symptomatic GBS chorioamnionitis. It has been shown that when the amniotic fluid concentration of GBS is high (>106 colony-forming units per ml), a few doses of intravenous ampicillin given to the mother will not necessarily sterilize the amniotic fluid (13). However, therapeutic fetal serum levels of ampicillin are achieved within hours after a single maternal dose (22). Various risk factors have been identified for selection of patients who are most likely to benefit from intrapartum antibiotic chemoprophylaxis (Table 1). They include maternal colonization with GBS plus: * Preterm labor (<37 weeks), or * Preterm premature rupture of membranes (<37 weeks), or * Prolonged rupture of membranes (>18 hours), or * Sibling affected by symptomatic GBS infection, or * Maternal fever during labor While studies have demonstrated the effectiveness of intrapartum chemoprophylaxis for high-risk situations (Table 1), no authorities presently recommend intrapartum chemoprophylaxis for all pregnant women colonized with GBS (approximately 20% of women in labor). If a rapid antigen test for GBS with sensitivity, specificity, and practicality comparable to those of conventional culture were available it would be useful particularly when these clinical risk factors are present and the status of GBS colonization is unknown. When a clinical risk factor is present but the culture result is unavailable and a rapid test cannot be performed, it may be reasonable to use antibiotic chemoprophylaxis empirically (23). If tests later prove to be negative for GBS or positive for a different bacterium, then the antibiotic regimen can be changed as indicated or discontinued. Treatment Antibiotic therapy should be started for any GBS-positive woman who becomes febrile during labor. The indicated treatment for symptomatic GBS infection of mother or baby is penicillin or ampicillin. Erythromycin or clindamycin may be used for mothers who are allergic to penicillin or ampicillin. Broader antibiotic regimens should be considered when treating chorioamnionitis in order to cover both GBS and additional penicillin-resistant bacteria (eg, anaerobic and gram-negative bacilli) that are likely to be present. Newborns do not develop allergies to penicillin or ampicillin; therefore, neonates may be treated with parenteral penicillin or ampicillin. When postpartum GBS endomyometritis is being treated, antibiotics should be continued until the patient has been afebrile and free of symptoms for at least 24 hours. Summary GBS is the leading cause of perinatal bacterial infections in the United States. Selective intrapartum chemoprophylaxis can prevent GBS early-onset neonatal disease and reduce maternal puerperal morbidity. There does not appear to be an effect on late-onset neonatal disease. Protocols for intrapartum antibiotic chemoprophylaxis based on antepartum cultures, testing at parturition, and clinical risk factors have been summarized. While screening of all pregnant women for GBS is an option, screening and selection methods need further development. A highly reliable rapid screening test for intrapartum detection of light and heavy GBS colonization of the lower genital tract is not yet available. Intrapartum antibiotic chemoprophylaxis of GBS carriers with one or more risk factors substantially re-duces the frequency of GBS disease. Benefit may also be obtained from prophylaxis based solely on a knowledge of risk factors if GBS carrier status is unknown. The importance of GBS infection as a perinatal problem and its considerable economic burden justify implementation of chemoprophylactic programs by obstetricians, particularly those who encounter a high proportion of patients with perinatal risk factors in their practices. REFERENCES 1. Baker CJ. Summary of the workshop on perinatal infections due to group B streptococcus. J Infect Dis 1977;136: 137-152 2. Faro S. Group B beta-hemolytic streptococci and puerperal infections. Am J Obstet Gynecol 1981;139:686-689 3. Regan JA, Chao S, James LS. Premature rupture of membranes, preterm delivery, and group B streptococcal colonization of mothers. Am J Obstet Gynecol 1981;141: 184-186 4. Alger LS, Lovchik JC, Hebel JR, Blackmon LR, Crenshaw MC. The association of Chlamydia trachomatis, Neisseria gonorrhoeae, and group B streptococci with preterm rupture of the membranes and pregnancy outcome. Am J Obstet Gynecol 1988;159:397-404 5. Thomsen AC, Morup L, Hansen KB. Antibiotic elimination of group-B streptococci in urine in prevention of preterm labour. Lancet 1987;1:591-593 6. Gardner SE, Yow MD, Leeds LJ, Thompson PK, Mason EO Jr, Clark DJ. Failure of penicillin to eradicate group B streptococcal colonization in the pregnant woman. A couple study. Am J Obstet Gynecol 1979;135:1062-1065 7. Carey JC, Klebanoff MA, Regan JA. Evaluation of the Gram stain as a screening tool for maternal carriage of group B beta-hemolytic streptococci. The Vaginal Infections and Prematurity Group. Obstet Gynecol 1990;76: 693-697 8. Anthony BF, Eisenstadt R, Carter J, Kim KS, Hobel CJ. Genital and intestinal carriage of group B streptococci during pregnancy. J Infect Dis 1981; 143:761-766 9. Isada NB, Grossman JH III. A rapid screening test for the diagnosis of endocervical group B streptococci in pregnancy: microbiologic results and clinical outcome. Obstet Gynecol 1987;70:139-141 10. Schuchat A, Oxtoby M, Cochi S, Sikes RK, Hightower A, Plikaytis B, Broome CV. Population-based risk factors for neonatal group B streptococcal disease: results of a cohort study in metropolitan Atlanta. J Infect Dis 1990;162:672-677 11. Boyer KM, Gotoff SP. Prevention of early-onset neonatal group B streptococcal disease with selective intrapartum chemoprophylaxis. N Engl J Med 1986;314: 1665-1669 12. Tuppurainen N, Hallman M. Prevention of neonatal group B streptococcal disease: intrapartum detection and chemoprophylaxis of heavily colonized parturients. Obstet Gynecol 1989;73:583-587 13. Silver HM, Gibbs RS, Gray BM, Dillon HC. Risk factors for perinatal group B streptococcal disease after amniotic fluid colonization. Am J Obstet Gynecol 1990;163: 19-25 14. Baker CJ, Barrett FF, Yow MD. The influence of advancing gestation on group B streptococcal colonization in pregnant women. Am J Obstet Gynecol 1975;122:820-823 15. Morales WJ, Lim D. Reduction of group B streptococcal maternal and neonatal infections in preterm pregnancies with premature rupture of membranes through a rapid identification test. Am J Obstet Gynecol 1987;157:13-16 16. Minkoff HL, Sierra MF, Pringle GF, Schwarz RH. Vaginal colonization with group B beta-hemolytic streptococcus as a risk factor for post-cesarean section febrile morbidity. Am J Obstet Gynecol 1982;142:992-995 17. Brady K, Duff P, Schilhab JC, Herd M. Reliability of a rapid latex fixation test for detecting group B streptococci on the genital tract of parturients at term. Obstet Gynecol 1989;73:678-681 18. Towers CV, Garite TJ, Friedman WW, Pircon RA, Nageotte MP. Comparison of a rapid enzyme-linked immunosorbent assay test and the Gram stain for detection of group B streptococcus in high-risk antepartum patients. Am J Obstet Gynecol 1990;163:965-967 19. Strickland DM, Yeomans ER, Hankins GDV. Cost-effectiveness of intrapartum screening and treatment for maternal group B streptococci colonization. Am J Obstet Gynecol 1990;163:4-8 20. Merenstein GB, Todd WA, Brown G, Yost CC, Luzier T. Group B b-hemolytic streptococcus: randomized controlled treatment study at term. Obstet Gynecol 1980;55:315-318 21. Allardice JG, Baskett TF, Seshia MM, Bowman N, Malazdrewicz R. Perinatal group B streptococcal colonization and infection. Am J Obstet Gynecol 1982;142:617-620 22. Bray RE, Boe RW, Johnson WL. Transfer of ampicillin into fetus and amniotic fluid from maternal plasma late in pregnancy. Am J Obstet Gynecol 1966;96:938-942 23. Minkoff H, Mead P. An obstetric approach to the prevention of early-onset group B b-hemolytic streptococcal sepsis. Am J Obstet Gynecol 1986;154:973-977
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