Group B streptococcal infection natural history: Difference between revisions
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]; Associate Editor(s)-in-Chief: Rim Halaby, M.D. [3]
Overview
Group B Streptococcus (GBS) is the leading infectious cause of morbidity and mortality among infants in the United States, particularly among preterm neonates.[1][2][3] Most newborns with early-onset disease have symptoms on the day of birth. Babies who develop late-onset disease may appear healthy at birth and develop symptoms of GBS disease after the first week of life.
Natural History, Complications and Prognosis
GBS in Neonates
Natural History
Most newborns with early-onset disease have symptoms on the day of birth. Babies who develop late-onset disease may appear healthy at birth and develop symptoms of group B strep disease after the first week of life. Infants with early-onset GBS disease generally present with respiratory distress, apnea, or other signs of sepsis within the first 24 to 48 hours of life.[4] The most common clinical syndromes of early-onset disease are sepsis and pneumonia; less frequently, early-onset infections can lead to meningitis.
Complications
- Disseminated intravascular coagulation (DIC)
- Hypoglycemia
- Respiratory failure
- Neurological complications of meningitis
- Brain infarction
- Cerebral edema
- Cerebritis
- Elevated intracranial pressure
- Hydrocephalus
- Subdural effusion
- Subdural empyema
- Ventriculitis
- Death
Mortality
GBS is the leading infectious cause of morbidity and mortality among infants in the United States. The case-fatality ratio of early-onset disease has declined from as high as 50% in the 1970s[1] to 4%-6% in recent years, primarily because of advances in neonatal care.[2][3]
Mortality is higher among preterm infants, with case-fatality rates of approximately 20% and as high as 30% among those ≤33 weeks of gestation, compared with 2%--3% among full-term infants.[2][3]
GBS in Pregnancy
Natural History
GBS colonization during pregnancy can be transient, intermittent, or persistent. Although some women with GBS colonization during a pregnancy will be colonized during subsequent pregnancies, a substantial proportion will not.[5][6] In the absence of any intervention, an estimated 1%-2% of infants born to colonized mothers develop early-onset GBS infections.[7][8]
Pregnant women who are colonized by GBS are most commonly asymptomatic. Some pregnant women develop serious conditions as a result of the infection, such as endometritis, chorioamnionitis, urinary tract infections, and preterm delivery.
References
- ↑ 1.0 1.1 Baker CJ, Barrett FF (1974). "Group B streptococcal infections in infants. The importance of the various serotypes". JAMA. 230 (8): 1158–60. PMID 4608888.
- ↑ 2.0 2.1 2.2 Phares CR, Lynfield R, Farley MM, Mohle-Boetani J, Harrison LH, Petit S; et al. (2008). "Epidemiology of invasive group B streptococcal disease in the United States, 1999-2005". JAMA. 299 (17): 2056–65. doi:10.1001/jama.299.17.2056. PMID 18460666.
- ↑ 3.0 3.1 3.2 Schrag SJ, Zywicki S, Farley MM, Reingold AL, Harrison LH, Lefkowitz LB; et al. (2000). "Group B streptococcal disease in the era of intrapartum antibiotic prophylaxis". N Engl J Med. 342 (1): 15–20. doi:10.1056/NEJM200001063420103. PMID 10620644.
- ↑ Franciosi RA, Knostman JD, Zimmerman RA (1973). "Group B streptococcal neonatal and infant infections". J Pediatr. 82 (4): 707–18. PMID 4572747.
- ↑ Cheng PJ, Chueh HY, Liu CM, Hsu JJ, Hsieh TT, Soong YK (2008). "Risk factors for recurrence of group B streptococcus colonization in a subsequent pregnancy". Obstet Gynecol. 111 (3): 704–9. doi:10.1097/AOG.0b013e318163cd6b. PMID 18310374.
- ↑ Turrentine MA, Ramirez MM (2008). "Recurrence of group B streptococci colonization in subsequent pregnancy". Obstet Gynecol. 112 (2 Pt 1): 259–64. doi:10.1097/AOG.0b013e31817f5cb9. PMID 18669720.
- ↑ CDC. Prevention of perinatal group B streptococcal disease: a public health perspective. MMWR 1996;45(No. RR-7).[1]
- ↑ Boyer KM, Gotoff SP (1985). "Strategies for chemoprophylaxis of GBS early-onset infections". Antibiot Chemother (1971). 35: 267–80. PMID 3931544.