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Search: WFRF:(Oler E.)

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  • Walker, C. L., et al. (author)
  • Ultrasound prediction of Zika virus-associated congenital injury using the profile of fetal growth
  • 2020
  • In: PLoS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 15:5
  • Journal article (peer-reviewed)abstract
    • Zika virus (ZIKV) is a mosquito-transmitted flavivirus, recently linked to microcephaly and central nervous system anomalies following infection in pregnancy. Striking findings of disproportionate growth with a smaller than expected head relative to body length have been observed more commonly among fetuses with exposure to ZIKV in utero compared to pregnancies without ZIKV infection regardless of other signs of congenital infection including microcephaly. This study's objective was to determine the diagnostic accuracy of femursparing profile of intrauterine growth restriction for the identification of ZIKV-associated congenital injuries on postnatal testing. A retrospective cohort study of pregnant women with possible or confirmed ZIKV infection between January 1, 2016 and December 31, 2017 were included. Subjects were excluded if no prenatal ultrasound was available. A femursparing profile of growth restriction determined using INTERGROWTH-21st sonographic standard for head circumference to femur length (HC: FL). Congenital injuries were determined postnatally by imaging, comprehensive eye exam and standard newborn hearing screen. A total of 111 pregnant women diagnosed with ZIKV infection underwent fetal ultrasound and 95 neonates had complete postnatal evaluation. Prenatal microcephaly was detected in 5% of fetuses (6/111). Postnatal testing detected ZIKV-associated congenital injuries in 25% of neonates (24/95). A HC: FL Z-score <=-1.3 had a 52% specificity (95% CI 41-63%), 82% negative predictive value (NPV, 95% CI 73-88%) for the detection of ZIKV-associated congenital injuries in the neonatal period. A more stringent threshold with a Z-score <=-2 was associated with a 90% specificity (95% CI 81-95%), 81% NPV (95% CI 77-85%). Excluding cases of fetal microcephaly, HC: FL (Z-score <=-2) demonstrated a similar specificity (89%, 95% CI 81-95%) with superior NPV (87%, 95% CI 84-90%). The sono-graphic recognition of a normally proportioned fetus may be useful prenatally to exclude a wider spectrum of ZIKV-associated congenital injuries detected postnatally.
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3.
  • Armistead, B., et al. (author)
  • The Double Life of Group B Streptococcus: Asymptomatic Colonizer and Potent Pathogen
  • 2019
  • In: Journal of Molecular Biology. - : Elsevier BV. - 0022-2836. ; 431:16, s. 2914-2931
  • Research review (peer-reviewed)abstract
    • Group B streptococcus (GBS) is a β-hemolytic gram-positive bacterium that colonizes the lower genital tract of approximately 18% of women globally as an asymptomatic member of the gastrointestinal and/or vaginal flora. If established in other host niches, however, GBS is highly pathogenic. During pregnancy, ascending GBS infection from the vagina to the intrauterine space is associated with preterm birth, stillbirth, and fetal injury. In addition, vertical transmission of GBS during or after birth results in life-threatening neonatal infections, including pneumonia, sepsis, and meningitis. Although the mechanisms by which GBS traffics from the lower genital tract to vulnerable host niches are not well understood, recent advances have revealed that many of the same bacterial factors that promote asymptomatic vaginal carriage also facilitate dissemination and virulence. Furthermore, highly pathogenic GBS strains have acquired unique factors that enhance survival in invasive niches. Several host factors also exist that either subdue GBS upon vaginal colonization or alternatively permit invasive infection. This review summarizes the GBS and host factors involved in GBS's state as both an asymptomatic colonizer and an invasive pathogen. Gaining a better understanding of these mechanisms is key to overcoming the challenges associated with vaccine development and identification of novel strategies to mitigate GBS virulence. © 2019 Elsevier Ltd
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