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Streptococcal Infection in Pregnancy |
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Group B Streptococcal Infection in Pregnancy In recent years, little progress has been achieved against perinatal group B streptococcus (GBS) infection. The bacteria remains a major cause of neonatal morbidity and mortality in the United States. Currently, the problem is managed through prophylactic antibiotic administration to highrisk women. Further progress against the disease awaits advances in immunology. Since 1938, Group B streptococcus has been recognized as a human pathogen (Chapman, 1986, p. 404). Fry (1938) described 3 cases of puerperal sepsis involving the microorganism. More recently, GBS has been established as a major cause of infection in women and neonates. In general, bacterial species responsible for neonatal infection tend to exhibit geographic variation. Streptococci of Lancefield group B (species, Streptococcus agalactiae) are the predominant cause of neonatal invasive disease in the U.S. Indeed, in this country GBS is the most common cause of neonatal sepsis and purulent meningitis. Furthermore, despite the administration of antimicrobial therapies and improvements in intensive care, the outcome for this infection remains serious (Givner & Baker, 1988, p. 65). Thus, considerable attention has been focused upon the possibility of preventing GBS infections. Problems associated with GBS may include maternal chorioamnionitis and endomyometritis. This pathology results from ascending infection. Moreover, the maternal genital tract ma
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labor; (5) premature rupture of membranes; (6) intrapartum fever; (7) multiple gestation; (8) incompetent cervix; (9) suspected amnionitis; (10) lack of immunity; (11) and diabetes (Hueston, 1991, p. 489). Venereal diseases which frequently accompany GBS colonization include Mycoplasma and Chlamydia (Fuller, 1992, p. 489). Furthermore, the sexual partners of these women may also be infected; the colonization rate for carriers' partners is approximately 50%.
Although maternal transmission of GBS to the neonate most frequently occurs as it passes through the birth canal, this particular route is rarely associated with pathological consequences. In fact, most earlyonset GBS disease is caused by ascending infection, with invasion of the intrauterine cavity subsequent to membrane rupture. Thus, increased lengths of time between placental membrane rupture and delivery give group B streptococci more of a chance to spread.
When maternal infection is symptomatic it may be manifested by such problems as chorioamnionitis, endomyometritis, cystitis, and pyelonephritis. One risk factor for postpartum endomyometritis is cesarean delivery. Yet another possible maternal complication is postpartum fever. The severity of these
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Tech Bull, Academy Sciences, Givner Baker, Garland Fliegner, Chlamydia Fuller, Lateonset GBS, Neonatal GBS, United Currently, Streptococci Lancefield, Infection Pregnancy, gbs infection, gbs disease, acog tech bull, tech bull, acog tech, bull #170, tech bull #170, bull #170 1993, #170 1993, fuller 1992, pregnant women, hueston 1991, earlyonset gbs disease, givner baker, #170 1993 55,
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