Shiloh
Editor, Senior Moderator
Source: http://www.cidrap.umn.edu/news-perspective/2017/04/stewardship-resistance-scan-apr-18-2017
Stewardship / Resistance Scan for Apr 18, 2017
Azithromycin and abnormal heartbeat; Mutations in resistant bacteria
Filed Under:
Antimicrobial Stewardship
[h=3]Azithromycin not found to increase risk of ventricular arrhythmia[/h] A study today in the Canadian Medical Association Journal (CMAJ) has found that use of the antibiotic azithromycin was associated with increased risk of ventricular arrhythmia (abnormal heartbeat) when compared with nonuse of antibiotics, but not when compared with use of amoxicillin.
In the nested case-control study, a team of European researchers used healthcare databases from Italy, the United Kingdom, Germany, the Netherlands, and Denmark to identify patients with ventricular arrhythmia who were new antibiotic users. They were looking to see if there is a link between the use of azithromycin?an antibiotic commonly used to treat respiratory and urinary tract infections?and increased risk of death from ventricular arrhythmia. Concerns about a potential link have been raised by the arrhythmogenic risk associated with another macrolide, erythromycin, but observational studies have to date produced conflicting results.
Of the more than 14 million new antibiotic users identified, 12,874 (0.1%) developed ventricular arrhythmia, and 30 were current azithromycin users. In matching the 30 current azithromycin users with 1,344 case controls, the researchers found that, when compared with nonuse of antibiotics, current azithromycin use was associated with an increased risk of ventricular arrhythmia (adjusted odds ratio [OR] 1.97). But when compared with current use of amoxicillin, the increased risk disappeared (adjusted OR 0.94). The results were consistent across separate databases and 1- and 2-stage pooled analyses.
The authors of the study say the decreased risk with an active comparator "suggests significant confounding by indication," meaning that the risk of ventricular arrhythmia is more likely associated with the patient's infection than with the antibiotic being used.
"This finding suggests that the risk of ventricular arrhythmia is more likely to be due to a person's poor health and caused by their infection, rather than to azithromycin itself," study author Gianluca Trifiro, MD, from the University of Messina, Italy, said in CMAJ news release.
The authors note that because the study used data on community use of antibiotics, the findings should not be extrapolated to the hospital setting, where the health status of patients and the nature of antibiotic use are likely to be different.
Apr 18 CMAJ abstract
Apr 18 CMAJ news release
[h=3]Study identifies compensatory mutations in multidrug-resistant bacteria[/h] A study today in PLoS Biology suggests that multidrug-resistant bacteria acquire compensatory mutations faster than bacteria that are resistant to a single antibiotic, a finding researchers say could open up new paths for novel antimicrobial strategies.
Chromosomal mutations that confer resistance often come with a fitness cost for bacteria in the absence of antibiotics. To counter that fitness cost, bacteria acquire additional mutations, known as compensatory mutations, that enable them to survive and spread. While this evolutionary process has been studied in single-resistant strains, less is known about how multidrug-resistant bacteria acquire compensatory mutations.
In the study, researchers from the Instituto Gulbenkian de Ciencia in Portugal analyzed and compared, in an antibiotic-free medium, the evolution of strains of Escherichia coli with single resistance to rifampicin and streptomycin and strains with resistance to both antibiotics. What they found was that the low-fitness double-resistant E coli strains acquired compensatory mechanisms faster than the single-resistant strains, primarily because of the acquisition of mutations with larger effects.
In addition, the researchers identified mutations that only compensate for double resistance and likely compensate specifically for the interaction between drug resistances.
"Interestingly, this knowledge may provide new grounds for the development of novel antimicrobial strategies that specifically exploit potential weaknesses derived from epistasis between antibiotic resistances in multidrug-resistant bacteria," the authors write.
Apr 18 PLoS Biol study
Stewardship / Resistance Scan for Apr 18, 2017
Azithromycin and abnormal heartbeat; Mutations in resistant bacteria
Filed Under:
Antimicrobial Stewardship
[h=3]Azithromycin not found to increase risk of ventricular arrhythmia[/h] A study today in the Canadian Medical Association Journal (CMAJ) has found that use of the antibiotic azithromycin was associated with increased risk of ventricular arrhythmia (abnormal heartbeat) when compared with nonuse of antibiotics, but not when compared with use of amoxicillin.
In the nested case-control study, a team of European researchers used healthcare databases from Italy, the United Kingdom, Germany, the Netherlands, and Denmark to identify patients with ventricular arrhythmia who were new antibiotic users. They were looking to see if there is a link between the use of azithromycin?an antibiotic commonly used to treat respiratory and urinary tract infections?and increased risk of death from ventricular arrhythmia. Concerns about a potential link have been raised by the arrhythmogenic risk associated with another macrolide, erythromycin, but observational studies have to date produced conflicting results.
Of the more than 14 million new antibiotic users identified, 12,874 (0.1%) developed ventricular arrhythmia, and 30 were current azithromycin users. In matching the 30 current azithromycin users with 1,344 case controls, the researchers found that, when compared with nonuse of antibiotics, current azithromycin use was associated with an increased risk of ventricular arrhythmia (adjusted odds ratio [OR] 1.97). But when compared with current use of amoxicillin, the increased risk disappeared (adjusted OR 0.94). The results were consistent across separate databases and 1- and 2-stage pooled analyses.
The authors of the study say the decreased risk with an active comparator "suggests significant confounding by indication," meaning that the risk of ventricular arrhythmia is more likely associated with the patient's infection than with the antibiotic being used.
"This finding suggests that the risk of ventricular arrhythmia is more likely to be due to a person's poor health and caused by their infection, rather than to azithromycin itself," study author Gianluca Trifiro, MD, from the University of Messina, Italy, said in CMAJ news release.
The authors note that because the study used data on community use of antibiotics, the findings should not be extrapolated to the hospital setting, where the health status of patients and the nature of antibiotic use are likely to be different.
Apr 18 CMAJ abstract
Apr 18 CMAJ news release
[h=3]Study identifies compensatory mutations in multidrug-resistant bacteria[/h] A study today in PLoS Biology suggests that multidrug-resistant bacteria acquire compensatory mutations faster than bacteria that are resistant to a single antibiotic, a finding researchers say could open up new paths for novel antimicrobial strategies.
Chromosomal mutations that confer resistance often come with a fitness cost for bacteria in the absence of antibiotics. To counter that fitness cost, bacteria acquire additional mutations, known as compensatory mutations, that enable them to survive and spread. While this evolutionary process has been studied in single-resistant strains, less is known about how multidrug-resistant bacteria acquire compensatory mutations.
In the study, researchers from the Instituto Gulbenkian de Ciencia in Portugal analyzed and compared, in an antibiotic-free medium, the evolution of strains of Escherichia coli with single resistance to rifampicin and streptomycin and strains with resistance to both antibiotics. What they found was that the low-fitness double-resistant E coli strains acquired compensatory mechanisms faster than the single-resistant strains, primarily because of the acquisition of mutations with larger effects.
In addition, the researchers identified mutations that only compensate for double resistance and likely compensate specifically for the interaction between drug resistances.
"Interestingly, this knowledge may provide new grounds for the development of novel antimicrobial strategies that specifically exploit potential weaknesses derived from epistasis between antibiotic resistances in multidrug-resistant bacteria," the authors write.
Apr 18 PLoS Biol study