Faculty Bibliography

BACKGROUND AND OBJECTIVE/OBJECTIVE:Methicillin-resistant Staphylococcus aureus (MRSA) is a significant cause of morbidity and mortality in NICUs and PICUs. Our objective was to assess the burden of MRSA colonization on admission, study the time trends, and examine the significance of MRSA colonization in this population. METHODS:PubMed and Embase databases were consulted. Studies that reported prevalence of MRSA colonization on ICU admission were selected. Two authors independently extracted data on MRSA colonization and infection. RESULTS:We identified 18 suitable articles and found an overall prevalence of MRSA colonization of 1.9% (95% confidence interval [CI] 1.3%-2.6%) on admission to the NICU or PICU, with a stable trend over the past 12 years. Interestingly, 5.8% (95% CI 1.9%-11.4%) of outborn neonates were colonized with MRSA on admission to NICU, compared with just 0.2% (95% CI 0.0%-0.9%) of inborn neonates (P = .01). The pooled acquisition rate of MRSA colonization was 4.1% (95% CI 1.2%-8.6%) during the NICU and PICU stay and was as high as 6.1% (95% CI 2.8%-10.6%) when the NICU population was studied alone. There was a relative risk of 24.2 (95% CI 8.9-66.0) for colonized patients to develop a MRSA infection during hospitalization. CONCLUSIONS:In the NICU and PICU, there are carriers of MRSA on admission, and MRSA colonization in the NICU is almost exclusively associated with outborn neonates. Importantly, despite infection control measures, the acquisition rate is high, and patients colonized with MRSA on admission are more likely to suffer a MRSA infection during hospitalization.

It has been postulated that chromatin modifications can persist through mitosis and meiosis, thereby securing memory of transcriptional states. Whether these chromatin marks can self-propagate in progeny independently of relevant trans-acting factors is an important question in phenomena related to epigenesis. "Adaptive cellular memory" displayed by yeast cells offers a convenient system to address this question. The yeast GAL genes are slowly activated by Gal4 when cells are first exposed to galactose, but their progeny, grown in glucose media, exhibit a fast activation mode upon re-exposure to this sugar. This "galactose memory" persists for several generations and was recently proposed to involve chromatin modifications and perinuclear topology of the GAL genes cluster. Here, we perform a heterokaryon assay demonstrating that this memory does not have a chromatin basis but is maintained by cytoplasmic factor(s) produced upon previous galactose induction. We show that Gal3, the cytoplasmic rate-limiting factor that releases the Gal4 activator, is dispensable for preserving galactose memory. Instead, the important memory determinant is a close Gal3 homolog, the highly expressed Gal1 galactokinase, the residual activity of which preserves memory in progeny cells by rapidly turning on the Gal4 activator upon cells' re-exposure to galactose.