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1.  Vaginal-rectal colonization with group A streptococci in late pregnancy. 
OBJECTIVE: To determine the vaginal-rectal colonization rate with group A streptococci in late pregnancy. METHODS: All patients delivering at a northern New England hospital over a 38 month period had 35-37 week vaginal-rectal swabs cultured for group A and group B streptococci, using selective media and slide agglutination. RESULTS: Six thousand nine hundred forty-four screening cultures were obtained. Among these 1,393 were positive for group B streptococci and 2 for group A streptococci, yielding colonization rates of 20.1% and 0.03%, respectively. CONCLUSIONS: Vaginal-rectal colonization with group A streptococci is rare, arguing against the need for establishing group A streptococcal screening programs in pregnancy. An approach for managing this uncommon finding is presented.
PMCID: PMC1784695  PMID: 11220480
2.  Food-related illness and death in the United States. 
Emerging Infectious Diseases  1999;5(5):607-625.
To better quantify the impact of foodborne diseases on health in the United States, we compiled and analyzed information from multiple surveillance systems and other sources. We estimate that foodborne diseases cause approximately 76 million illnesses, 325,000 hospitalizations, and 5,000 deaths in the United States each year. Known pathogens account for an estimated 14 million illnesses, 60, 000 hospitalizations, and 1,800 deaths. Three pathogens, Salmonella, Listeria, and Toxoplasma, are responsible for 1,500 deaths each year, more than 75% of those caused by known pathogens, while unknown agents account for the remaining 62 million illnesses, 265,000 hospitalizations, and 3,200 deaths. Overall, foodborne diseases appear to cause more illnesses but fewer deaths than previously estimated.
PMCID: PMC2627714  PMID: 10511517
4.  International epidemiological and microbiological study of outbreak of Salmonella agona infection from a ready to eat savoury snack--I: England and Wales and the United States. 
BMJ : British Medical Journal  1996;313(7065):1105-1107.
OBJECTIVES: To identify the source of an international outbreak of food poisoning due to Salmonella agona phage type 15 and to measure how long the underlying cause persisted. DESIGN: Case-control study of 16 primary household cases and 32 controls of similar age and dietary habit. Packets of the implicated foodstuff manufactured on a range of days were examined for salmonella. All isolates of the epidemic phage type were further characterised by pulsed field gel electrophoresis. RESULTS: 27 cases were identified, of which 26 were in children. The case-control study showed a strong association between infection with S agona phage type 15 and consumption of a peanut flavoured ready to eat kosher savoury snack imported from Israel. S agona phage type 15 was isolated from samples of this snack. The combined food sampling results from the United Kingdom, Canada, the United States, and Israel showed that contaminated snacks were manufactured on at least seven separate dates during a four month period between October 1994 and February 1995. Voluntary recalls of the product successfully interrupted transmission. CONCLUSIONS: Rapid international exchanges of information led to the identification of the source of a major outbreak of S agona in Israel and of associated cases in North America. The outbreak showed the value of the Salm-Net surveillance system and its links outside Europe, both for increasing case ascertainment and for improving the information on the duration of the fault at the manufacturing plant.
PMCID: PMC2352464  PMID: 8916693
6.  The source of the circulating aggregate of insulin in type I diabetic patients is therapeutic insulin. 
Journal of Clinical Investigation  1986;77(3):717-723.
Circulating insulin immunoreactivity (IRI) in type I diabetic patients (insulin-dependent diabetes mellitus [IDDM]) includes a covalent aggregate about twice the size of insulin. These studies were designed to determine the source and conditions promoting the accumulation of this material. Among 31 IDDMs, the aggregate made up 28 +/- 3.6% of the mean fasting plasma IRI. Five of these patients were restudied after 5 d of treatment with equidose intravenous insulin. The relative amount of the aggregate during subcutaneous treatment (40 +/- 8.0%) was indistinguishable (P greater than 0.7) from that at the termination of intravenous treatment (41 +/- 6.8%). To determine whether previous exposure to therapeutic insulin influenced the appearance and accumulation of the aggregate, we intravenously or subcutaneously infused insulin for 5 h in nine healthy volunteers (euglycemic clamp). At the termination of the high-dose intravenous infusion (10 mU X kg-1 X min-1), the concentration of the aggregate was 81 +/- 18 microU/ml, and it accounted for 2.9% of total IRI. At the conclusion of the other infusion protocols, the absolute amounts of aggregate were somewhat less, but they accounted for similar percentages. On polyacrylamide gel electrophoresis, the circulating aggregate was indistinguishable from a material of similar molecular weight contaminating commercial insulin. We conclude that the insulin aggregate found in the blood of IDDMs originates in commercial insulin. Its appearance is independent of the route of insulin administration. Prolonged and continuous use of insulin may increase its concentration but is not necessary for its appearance. The potential biologic and immunologic consequences of the aggregate are important matters that need to be addressed.
PMCID: PMC423455  PMID: 3512601
7.  Regulation of glucose utilization in adipose cells and muscle after long-term experimental hyperinsulinemia in rats. 
Journal of Clinical Investigation  1985;76(2):460-469.
The effects of chronic insulin administration on the metabolism of isolated adipose cells and muscle were studied. Adipose cells from 2 and 6 wk insulin-treated and control rats, fed either chow or chow plus sucrose, were prepared, and insulin binding, 3-O-methylglucose transport, glucose metabolism, and lipolysis were measured at various insulin concentrations. After 2 wk of treatment, adipose cell size and basal glucose transport and metabolism were unaltered, but insulin-stimulated transport and glucose metabolism were increased two- to threefold when cells were incubated in either 0.1 mM glucose (transport rate limiting) or 10 mM glucose (maximum glucose metabolism). Insulin binding was increased by 30%, but no shift in the insulin dose-response curve for transport or metabolism occurred. After 6 wk of treatment, the effects of hyperinsulinemia on insulin binding and glucose metabolism persisted and were superimposed on the changes in cell function that occurred with increasing cell size in aging rats. Hyperinsulinemia for 2 or 6 wk did not alter basal or epinephrine-stimulated lipolysis in adipose cells or the antilipolytic effect of insulin. In incubated soleus muscle strips, insulin-stimulated glucose metabolism was significantly increased after 2 wk of hyperinsulinemia, but these increases were not observed after 6 wk of treatment. We conclude that 2 wk of continuous hyperinsulinemia results in increased insulin-stimulated glucose metabolism in both adipose cells and soleus muscle. Despite increased insulin binding to adipose cells, no changes in insulin sensitivity were observed in adipose cells or muscle. In adipose cells, the increased glucose utilization resulted from both increased transport (2 wk only) and intracellular glucose metabolism (2 and 6 wk). In muscle, after 2 wk of treatment, both glycogen synthesis and total glucose metabolism were increased. These effects of hyperinsulinemia were lost in muscle after 6 wk of treatment, when compared with sucrose-supplemented controls.
PMCID: PMC423841  PMID: 3897286

Results 1-9 (9)