Background: Fluoroquinolones are often prescribed unnecessarily and are an important risk factor for infection with fluoroquinolone-resistant gram-negative bacilli and Clostridioides difficile. Methods: We conducted a quasi-experimental study to determine the impact of sequential syndrome-specific stewardship interventions on use of and resistance to fluoroquinolones in a tertiary care hospital. An initial 2-year intervention focused on reducing treatment of asymptomatic bacteriuria and ensuring concordance of urinary tract infection treatment with guidelines. A second 5-year intervention focused on limiting overuse of fluoroquinolones for health care−associated pneumonia in conjunction with a formal stewardship program. The primary outcomes were fluoroquinolone use and changes in use over time analyzed by segmented regression analysis. Results: The asymptomatic bacteriuria and urinary tract infection intervention resulted in a significant reduction in fluoroquinolone use, with a significant change from an increasing to a decreasing rate of use (change in slope of quarterly defined daily doses/1,000 patient days −15.3, P < .01). The health care−associated pneumonia intervention resulted in a continued significant reduction in fluoroquinolone use (rate ratio = 0.68, P < .01). During the interventions, fluoroquinolone susceptibility increased significantly in Pseudomonas aeruginosa, but not in Escherichia coli, Klebsiella spp., or C difficile. Conclusions: Antimicrobial stewardship interventions focused on specific syndromes may be effective in reducing fluoroquinolone use. In our hospital, reduction in fluoroquinolone use resulted in increased fluoroquinolone susceptibility in P aeruginosa, but not other Enterobacteriaceae or C difficile.
Carbapenem-resistant Enterobacteriaceae (CRE) usually infect patients with significant comorbidities and health care exposures. We present a case of a pregnant woman who developed community-acquired pyelonephritis caused by KPC-producing Klebsiella pneumoniae. Despite antibiotic treatment, she experienced spontaneous prolonged rupture of membranes, with eventual delivery of a healthy infant. This report demonstrates the challenge that CRE may pose to the effective treatment of common infections in obstetric patients, with potentially harmful consequences to maternal and neonatal health.
Objectives-Raised concentrations of antimony have been found in infants dying of sudden infant death syndrome (SIDS). The presumed source of this antimony is toxic gases generated from fire retardants that are present in cot mattresses. The aim of this study was to determine the role of antimony in SIDS. Design-Samples of liver, brain, serum, and urine were collected from all patients dying from SIDS and a group of aged matched control infants who had died of other causes. Setting-Nationwide study in Ireland. Subjects-52 infants dying from SIDS and 19 control infants aged > 7 days and < 1 year. Results-The median concentration of antimony in the liver and brain of infants dying of SIDS was < 1 ng/g, with no diVerence detected between the infants dying from SIDS and the control infants. The range of antimony in the serum of infants dying of SIDS was 0.09-0.71 µg/ litre (median, 0.26). Although no diVerence was found between infants dying from SIDS and control infants, SIDS infants were found to have higher concentrations when compared with healthy infants in the 1st year of life, probably as a result of release of antimony into serum after death. Urine antimony concentrations in infants dying from SIDS were < 3.91 ng/mg (corrected for creatinine) and similar to values found both in control infants and healthy infants. Conclusion-There is no evidence to support a causal role for antimony in SIDS.
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