Lessons Learned from a Decade of Investigations of Shiga Toxin-Producing Escherichia coli Outbreaks Linked to Leafy Greens, United States and Canada.

Shiga toxin-producing Escherichia coli (STEC) cause substantial and costly illnesses. Leafy greens are the second most common source of foodborne STEC O157 outbreaks. We examined STEC outbreaks linked to leafy greens during 2009-2018 in the United States and Canada. We identified 40 outbreaks, 1,212 illnesses, 77 cases of hemolytic uremic syndrome, and 8 deaths. More outbreaks were linked to romaine lettuce (54%) than to any other type of leafy green. More outbreaks occurred in the fall (45%) and spring (28%) than in other seasons. Barriers in epidemiologic and traceback investigations complicated identification of the ultimate outbreak source. Research on the seasonality of leafy green outbreaks and vulnerability to STEC contamination and bacterial survival dynamics by leafy green type are warranted. Improvements in traceability of leafy greens are also needed. Federal and state health partners, researchers, the leafy green industry, and retailers can work together on interventions to reduce STEC contamination.

Outbreak of Salmonella Chailey Infections Linked To Precut Coconut Pieces - United States and Canada, 2017.

Foodborne salmonellosis causes an estimated 1 million illnesses and 400 deaths annually in the United States (1). In recent years, salmonellosis outbreaks have been caused by foods not typically associated with Salmonella. On May 2, 2017, PulseNet, CDC's national molecular subtyping network for foodborne disease surveillance, identified a cluster of 14 Salmonella Chailey isolates with a rare pulsed-field gel electrophoresis (PFGE) pattern. On May 29, Canadian health officials informed CDC that they were also investigating a cluster of five Salmonella Chailey infections in British Columbia with the same PFGE pattern. Nineteen cases were identified and investigated by CDC, U.S. state health departments, the Public Health Agency of Canada, and the British Columbia Centre for Disease Control. Isolates from all cases were highly related by whole genome sequencing (WGS). Illness onset dates ranged from March 10 to May 7, 2017. Initial interviews revealed that infected persons consumed various fresh foods and shopped at grocery chain A; focused questionnaires identified precut coconut pieces from grocery chain A as a common vehicle. The Canadian Food Inspection Agency (CFIA) and the U.S. Food and Drug Administration (FDA) conducted a traceback investigation that implicated a single lot of frozen, precut coconut as the outbreak source. Grocery chain A voluntarily removed precut coconut pieces from their stores. This action likely limited the size and scope of this outbreak.

Outbreak of Vibrio parahaemolyticus Associated with Consumption of Raw Oysters in Canada, 2015.

There has been a steady increase in illness incidence of Vibrio parahaemolyticus (Vp). The majority of illnesses are associated with consumption of raw oysters. In the summer of 2015, Canada experienced the largest outbreak associated with the consumption of raw oysters harvested from British Columbia (BC) coastal waters. Case investigation of laboratory-confirmed cases was conducted to collect information on exposures and to assist traceback. Investigations at processors and oyster sampling were conducted. Eighty-two laboratory-confirmed cases of Vp infection were reported between January 1 and October 26, 2015. The majority of the cases were reported in BC, associated with consumption of raw BC oysters in restaurants. Sea surface temperatures were above the historical levels in 2015. This outbreak identified the need to improve surveillance and response to increases in human cases of Vp. This is of particular importance due to the potential for increasing water temperatures and the likelihood of additional outbreaks of Vibrio.

Poor Sleep Quality Is Associated with Higher Hemoglobin A1c in Pregnant Women: A Pilot Observational Study.

We hypothesized that poor sleep quality exacerbates glucose intolerance manifested as elevated glycosylated hemoglobin (HbA1c), which increases the risk for gestational diabetes. To test this, 38 pregnant and 22 non-pregnant (age, 18⁻35 years; body-mass index, 20⁻35 kg/m²) otherwise healthy women were enrolled in the study. Sleep quality was assessed during gestational week 24 (pregnant), or outside of the menstrual period (non-pregnant), using qualitative (Pittsburgh Sleep Quality Index) and objective (actigraphic wrist-watch) measures. Blood glucose, total cortisol, and depression status were evaluated. Eight pregnant and one non-pregnant women were lost to follow-up, or withdrew from the study. There was a higher incidence of poor sleep quality in pregnant (73%) relative to non-pregnant women (43%). Although actigraphic data revealed no differences in actual sleep hours between pregnant and non-pregnant women, the number of wake episodes and sleep fragmentation were higher in pregnant women. Poor sleep quality was positively correlated with higher HbA1c in both pregnant (r = 0.46, n = 26, p = 0.0151) and non-pregnant women (r = 0.50, n = 19, p = 0.0217), reflecting higher average blood glucose concentrations. In contrast, poor sleep was negatively correlated with cortisol responses in pregnant women (r = -0.46, n = 25, p = 0.0167). Three pregnant women had elevated one-hour oral glucose tolerance test results (>153 mg/dL glucose). These same pregnant women exhibited poor sleep quality. These results support the suggestion that poor sleep quality is an important risk factor that is associated with glucose intolerance and attendant health complications in pregnancy.

Effects of vitamin E on oxidative stress and atherosclerosis in an obese hyperlipidemic mouse model.

Vitamin E is a natural antioxidant that has been used in animal and human studies to determine its potential in reducing cardiovascular risk; however, a detailed study in an established obese model of atherosclerosis has yet to be performed. In our current study, we show that obesity and hyperlipidemia cause a synergistic, age-related increase in urinary isoprostane levels in mice deficient in both leptin and low-density lipoprotein receptor (ob/ob;LDLR-/-). Based upon this observation, we hypothesized that vitamin E supplementation would induce potent antiatherogenic effects in this model. Lean and obese LDLR-/- mice were provided vitamin E (2000 IU/kg) in a Western-type high-fat diet for 12 weeks. Plasma lipid parameters, such as total cholesterol (TC), triglyceride (TG) and free fatty acid, were significantly higher in obese mice compared to lean mice at baseline (P<.001). Western-type diet (WD) feeding caused an increase in TC levels in all groups (P<.001); however, TG (P<.001) and free fatty acid (P<.01) were elevated only in lean mice following WD feeding. Vitamin E supplementation neither influenced any of these parameters nor reduced urinary isoprostanes in lean or obese mice. Vitamin E supplementation in ob/ob;LDLR-/- mice resulted in a trend toward a reduction in atherosclerotic lesion area (P=.10), although no differences in lesion area were noted in lean LDLR-/- animals. These data provide evidence that vitamin E supplementation is not sufficient to reduce extreme elevations in systemic oxidative stress due to hyperlipidemia and obesity and, thus, may not be cardioprotective in this setting.

Macrophage-derived apolipoprotein E ameliorates dyslipidemia and atherosclerosis in obese apolipoprotein E-deficient mice.

Previous studies have demonstrated that macrophage-derived apolipoprotein E (apoE) reduces atherosclerotic lesion formation in lean apoE-deficient ((-/-)) mice. apoE has also been demonstrated to play a role in adipocyte differentiation and lipid accumulation. Because the prevalence of obesity has grown to epidemic proportions, we sought to determine whether macrophage-derived apoE could impact atherosclerotic lesion formation or adipose tissue expansion and inflammation in obese apoE(-/-) mice. To this end, we transplanted obese leptin-deficient (ob/ob) apoE(-/-) mice with bone marrow from either ob/ob;apoE(-/-) or ob/ob;apoE(+/+) donors. There were no differences in body weight, total body adipose tissue, or visceral fat pad mass between recipient groups. The presence of macrophage-apoE had no impact on adipose tissue macrophage content or inflammatory cytokine expression. Recipients of apoE(+/+) marrow demonstrated 3.7-fold lower plasma cholesterol (P < 0.001) and 1.7-fold lower plasma triglyceride levels (P < 0.01) by 12 wk after transplantation even though apoE was present in plasma at concentrations <10% of wild-type levels. The reduced plasma lipids reflected a dramatic decrease in very low density lipoprotein and a mild increase in high-density lipoprotein levels. Atherosclerotic lesion area was >10-fold lower in recipients of ob/ob;apoE(+/+) marrow (P < 0.005). Similar results were seen in leptin receptor-deficient (db/db) apoE(-/-) mice. Finally, when bone marrow transplantation was performed in 4-mo-old ob/ob;apoE(-/-) and db/db;apoE(-/-) mice with preexisting lesions, recipients of apoE(+/+) marrow had a 2.8-fold lower lesion area than controls (P = 0.0002). These results demonstrate that macrophage-derived apoE does not impact adipose tissue expansion or inflammatory status; however, even very low levels of macrophage-derived apoE are capable of reducing plasma lipids and atherosclerotic lesion area in obese mice.

The role of macrophage leptin receptor in aortic root lesion formation.

Plasma leptin is often elevated in obese individuals, and previous studies have suggested leptin as a factor that links obesity and atherosclerosis. Because macrophages play a key role in atherogenesis and are responsive to leptin, we hypothesized that leptin increases aortic root lesion formation, in part, through macrophage leptin receptor (LepR). Three different bone marrow transplantation studies were conducted in which bone marrow, with or without LepR, was transplanted into lethally irradiated 1) LDL receptor-deficient (LDLR(-/-)) mice with moderate hyperleptinemia due to Western diet (WD) feeding, 2) LDLR(-/-) mice with WD feeding plus pharmacologically induced hyperleptinemia (daily injection of 125 microg leptin), or 3) obese, hyperleptinemic, LepR-deficient LDLR(-/-) (LepR(db/db);LDLR(-/-)) mice. Minor differences in plasma parameters such as cholesterol, triglycerides, and insulin were observed in some groups; however, a consistent trend for the role of LepR on these parameters was not detected. In each of the studies, macrophage LepR expression did not have an effect on aortic root atherosclerotic lesion formation. These results suggest that nonhematopoietic cells may have a more significant role than macrophages in leptin-mediated effects on aortic root lesion formation.