We examined the frequency of acquisition of bacterial pathogens on investigators' hands after contacting environmental surfaces near hospitalized patients. Hand imprint cultures were positive for one or more pathogens after contacting surfaces near 34 (53%) of 64 study patients, with Staphylococcus aureus and vancomycin-resistant Enterococcus being the most common isolates.

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Intestinal colonization by methicillin-resistant Staphylococcus aureus (MRSA) is common in some groups of hospitalized patients and has been associated with an increased risk of staphylococcal infection. We tested the hypothesis that growth of MRSA in the colonic mucus layer is required for establishment of intestinal colonization. Mice treated with oral streptomycin before oral administration of MRSA developed persistent intestinal colonization, and the cecal mucus layer contained high concentrations of MRSA. MRSA strains grew rapidly when inoculated into cecal mucus in vitro but were unable to replicate under anaerobic conditions in cecal contents of saline- or streptomycin-treated mice. Oral vancomycin treatment reduced the density of 1 MRSA strain in stool but had no effect on a second strain. These results suggest that the cecal mucus layer provides an important niche that facilitates intestinal colonization by MRSA. Oral nonabsorbed antibiotics may be ineffective in eradicating some MRSA strains from the intestinal tract.

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A 26-year-old female with a history of preterm labor and cerclage placement presented at 29 weeks gestation. Twin girls were delivered at 29 1 7 weeks. Twin A presented with clinical sepsis at birth. Twin A's blood cultures became positive for Actinomyces species on day of life 15. Despite aggressive medical management twin A died at 35 days of life.

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This study tested the hypothesis that inhaled nitric oxide (NO) and combined NO and hyperoxia will result in less pulmonary dysfunction and delay onset of respiratory signs compared with hyperoxia-exposed newborn guinea pigs (GPs). GPs were exposed to room air (n = 14), 95% O(2) (n = 36), 20 parts per million (ppm) NO (n = 14), or combined 20 ppm NO and 95% O(2) (NO/O(2), n = 13) for up to 5 days. Data evaluated included latency interval for onset of respiratory distress, pressure volume curves, lung histology, and bronchoalveolar lavage (BAL) polymorphonuclear cells (PMNs), proteolytic activity, and total protein. NO-exposed GPs did not develop respiratory distress and had no evidence of pulmonary dysfunction. O(2)-exposed GPs developed respiratory distress after 1-5 days (median 4.0) vs. 3-5 days (median 5.0) for NO/O(2) exposure (P < 0.05). BAL from O(2)-exposed GPs showed increased PMNs compared with NO/O(2)-exposed GPs. O(2)- and NO/O(2)-exposed GPs had comparable reduced lung volumes, lung histology, and increased BAL proteinase activity and total protein. In summary 1) O(2) exposure resulted in multiple measures of pulmonary dysfunction in newborn GPs, 2) 5-day exposure to NO produced no noticeable respiratory effects and pulmonary dysfunction, and 3) short-term exposure (

This study was designed to test the hypotheses that furosemide directly causes relaxation in human fetal airway and that delivery of loop diuretics to either the adventitial or epithelial surface of newborn mouse airway results in equivalent relaxation. Isometric tension changes were measured in human fetal (11-16 wk) trachea and mainstem bronchus rings exposed to furosemide (300 M) or saline after acetylcholine or leukotriene D 4 constriction. Significant decreases in isometric tension to furosemide were demonstrated after constriction with acetylcholine or leukotriene D 4 . To examine the site of effect and mimic aerosolized and systemic administration, furosemide (3-300 M) and bumetanide (0.3-30 M) were applied separately to epithelial and adventitial surfaces of newborn mouse airways. No differences in airway diameter changes to epithelial or adventitial furosemide or bumetanide were observed, but a 10-fold difference in potency was found. In summary, human fetal airway relaxed to furosemide when constricted with either neurotransmitter or inflammatory mediator in vitro. Further, no differences in relaxation to equimolar epithelial and adventitial furosemide were observed in isolated newborn mouse airway. Taken together, this provides evidence that furosemide has a direct, nonepithelial-dependent effect on airway smooth muscle tone. Systemically administered furosemide improves pulmonary mechanics and gas exchange in infants with chronic lung disease independent of its diuretic effects (1, 2). Studies demonstrating a reduction of bronchoconstrictive responses in pediatric (3) and adult asthmatics (4, 5) with aerosolized furosemide further support the notion that a nondiuretic effect may produce improvements in pulmonary function. Indeed, the in vitro airway relaxation to furosemide that is observed in animal models (6 -8) suggests that there may be a direct effect on airway smooth muscle.However, a bronchodilatory response to inhaled furosemide is not consistently observed in infants with chronic lung disease (9, 10). Although aerosolized administration of furosemide could minimize systemic effects while producing localized bronchodilation, it is not widely accepted that inhaled furosemide has therapeutic efficacy during acute bronchoconstriction. Taken together, it is presently unclear whether these inconsistent results are because of species differences or inadequate concentrations of drug that reach the airway with aerosolized treatment, or because furosemide in fact does not act via a mechanism of direct airway smooth muscle relaxation (11). Therefore, the potential relevance of previous in vitro animal findings requires validation by the study of human airway response (12), with the first objective to test the hypothesis that furosemide causes direct relaxation of human fetal airway.In addition to demonstrating a direct relaxing effect on airway smooth muscle, further support for the bronchodilatory response to furosemide via aerosolization would require evidence that mechanisms can be activated from th...