Our weekly wrap-up of antimicrobial stewardship & antimicrobial resistance scans
Swiss researchers report MCR-1 in E coli from a urinary tract infection
Researchers in Switzerland yesterday reported they detected the MCR-1 resistance gene in a single Escherichia coli isolate collected from samples of human urinary tract infections. The research appeared in the International Journal of Infectious Diseases.
The study was the first prospective analysis of the prevalence of both MCR-1 and MCR-2 genes—which can transfer resistance to the last-resort antibiotic colistin to different types of bacteria—in human clinical samples, the authors said.
The researchers screened 2,049 enterobacterial isolates from two Swiss laboratories first for colistin resistance, then for the presence of MCR-1 and MCR-2. While 6 of the isolates (2 E coli, 2 Klebsiella pneumoniae, 1 Hafnia alvei, and 1 Salmonella isolate) were found to be colistin resistant, none of them tested positive for MCR-like genes. A single E coli strain that was susceptible to colistin, however, tested positive for MCR-1.
The researchers said the low prevalence rate of plasmid-mediated colistin resistance in the human clinical samples, despite the fact that colistin is used widely in Switzerland to treat infected animals, suggests that a high transfer of MCR-like genes from humans to animals has not yet occurred and might be possible to prevent. But the fact that MCR-1 was found in a colistin-susceptible E coli isolate indicates the gene might spread silently. To combat this, they urged large and regular screening of animal isolates.
The MCR-1 gene was first identified in E coli samples from food, animals, and patients in China in November 2015. Since then it has been detected in more than 30 countries. MCR-1–positive E coli has been previously found in Swiss hospital patients and in Swiss food.
MCR-2 was first detected in E coli isolates from Belgian pigs last month.
Aug 18 Int J Infect Dis abstract
Jul 7 CIDRAP News story on MCR-1 in Belgian pigs
Study profiles impact of antimicrobial-resistant bloodstream infections within Europe
Originally published Aug 18.
A new study of European hospitals is providing some perspective on the health and economic burden of bloodstream infections caused by antimicrobial-resistant bacteria.
The study, published today in Eurosurveillance, looked at data on more than 600,000 patients who experienced acute care episodes at 10 European hospitals in 2010 and 2011. The researchers sought to estimate the impact of bloodstream infections caused by third-generation cephalosporin-resistant Enterobacteriaceae (3GCRE), third-generation cephalosporin-susceptible Enterobacteriaceae (3GCSE), methicillin-resistant Staphylococcus aureus (MRSA), and methicillin-susceptible S aureus(MSSA) on hospital mortality, length of stay, and hospital costs. The hospitals were in Switzerland, France, Spain, Italy, Germany, and the United Kingdom.
Compared with non-infected patients, patients with bloodstream infections caused by 3GCRE, MRSA, and MSSA were significantly more likely to die in a hospital (with adjusted hazard ratios of 1.80, 2.42, and 1.81, respectively) and have prolonged hospital stays (9.3 days, 13.3 days, and 11.5 days). Bloodstream infections caused by 3GCSE significantly lengthened hospital stays, but not the risk of death.
Overall, bloodstream infections caused by S aureus had a greater effect on mortality, length of stay, and hospital costs per infection than infections caused by Enterobacteriaceae. But when the researchers compared the impact of resistant Enterobacteriaceae and S aureus bloodstream infections with those caused by susceptible strains, they found that third-generation cephalosporin resistance had a greater impact than methicillin resistance; 3GCRE infections significantly increased both the risk of death and the length of hospital stays compared with 3GCSE infections, while MRSA infections did not significantly increase the risk of death or length of hospitals stays compared with MSSA infections.
"Our data demonstrate the substantial health and economic burden imposed by BSI in European hospitals," the authors wrote.
Aug 18 Eurosurveill study
Study sheds more light on deadly MRSA complications in flu patients
Originally published Aug 15.
In an ongoing investigation into why secondary MRSA infections are often so fatal to patients with flu, researchers who did lab studies on mice found that flu infection alters the antibacterial response of white blood cells, prompting them to damage patients' lungs instead of the bacteria. The team from the University of Nebraska Medical Center and Albany Medical College described their findings today in the Journal of Experimental Medicine (JEM).
In an earlier study, one of the researchers had found mice with flu were susceptible to MRSA because the infection seemed to suppress the ability of macrophages and neutrophils to kill bacteria by releasing hydrogen peroxide and suppress other reactive oxygen species.
In the new study, researchers found that in coinfected mice, reactive oxygen species released by macrophages and neutrophils induced the death of inflammatory cells in the lungs, damaging surround tissue, according a press release today from Rockefeller University Press, the publisher of JEM. Also, they found that inhibiting NADPH oxidase 2 (Nox2), the enzyme that produces reactive oxygen species in macrophages and neutrophils, reduced lung damage and when added to antibiotics, improved survival of the mice.
Keer Sun, PhD, study coauthor and assistant professor at the University of Nebraska Medical Center, said in a press release, "Our results demonstrate that influenza infection disrupts the delicate balance between Nox2-dependent antibacterial immunity and inflammation. This not only leads to increased susceptibility to MRSA infection but also extensive lung damage." He said treatment that targets both MRSA and reactive oxygen species may yield important benefits for flu patients who have MRSA pneumonia.
Aug 15 J Exp Med abstract
Aug 15 Rockefeller University press release