The epidemiology of methicillin-resistant Staphylococcus aureus (MRSA) has changed dramatically over the past 15 years. Initially a nosocomial pathogen, newly emergent strains of MRSA have become increasingly common in the community among individuals lacking contact with healthcare. More recently, a third group of MRSA strains have been identified in association with livestock, particularly swine. These strains, termed livestock-associated MRSA, have now been identified in Europe, North America, and Asia in humans and animals. One molecular type, ST398, has been the dominant strain of livestock-associated MRSA identified to date. The emergence of this strain in animals and humans will be described in this review, including colonization and clinical infections caused by this strain. We also discuss lingering research questions and implications for controlling spread of this bacterium in an agricultural environment and beyond.

Risperidone is a second-generation antipsychotic that causes weight gain. We hypothesized that risperidone-induced shifts in the gut microbiome are mechanistically involved in its metabolic consequences. Wild-type female C57BL/6J mice treated with risperidone (80 μg/day) exhibited significant excess weight gain, due to reduced energy expenditure, which correlated with an altered gut microbiome. Fecal transplant from risperidone-treated mice caused a 16% reduction in total resting metabolic rate in naïve recipients, attributable to suppression of non-aerobic metabolism. Risperidone inhibited growth of cultured fecal bacteria grown anaerobically more than those grown aerobically. Finally, transplant of the fecal phage fraction from risperidone-treated mice was sufficient to cause excess weight gain in naïve recipients, again through reduced energy expenditure. Collectively, these data highlight a major role for the gut microbiome in weight gain following chronic use of risperidone, and specifically implicates the modulation of non-aerobic resting metabolism in this mechanism.

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Preeclampsia, a cardiovascular disorder of late pregnancy, is characterized as a low-renin hypertensive state relative to normotensive pregnancy. As other non-pregnant low-renin hypertensive disorders often exhibit and are occasionally dependent upon elevated arginine vasopressin (AVP) secretion, we hypothesized a possible use for plasma AVP measurements in the prediction of preeclampsia. Copeptin is an inert pro-segment of AVP that is secreted in a 1:1 molar ratio and exhibits a substantially longer biological half-life than AVP, rendering it a clinically useful biomarker of AVP secretion. Copeptin was measured throughout pregnancy in maternal plasma from preeclamptic and control women. Maternal plasma copeptin was significantly higher throughout preeclamptic pregnancies versus control pregnancies. While controlling for clinically significant confounders (age, BMI, chronic essential hypertension, twin gestation, diabetes, and history of preeclampsia) using multivariate regression, the association of higher copeptin concentration and the development of preeclampsia remained significant. Receiver operating characteristic analyses reveal that as early as the 6th week of gestation, elevated maternal plasma copeptin concentration is a highly significant predictor of preeclampsia throughout pregnancy. Finally, chronic infusion of AVP during pregnancy (24 ng/hr) is sufficient to phenocopy preeclampsia in C57BL/6J mice, causing pregnancy-specific hypertension, renal glomerular endotheliosis, proteinuria, and intrauterine growth restriction. These data (1) implicate AVP release as a novel predictive biomarker for preeclampsia very early in pregnancy, (2) identify chronic AVP infusion as a novel and clinically-relevant model of preeclampsia in mice, and are (3) consistent with a potential causative role for AVP in preeclampsia in humans.