scholarly journals Modeling the effect of vaccination on selection for antibiotic resistance in Streptococcus pneumoniae

2021 ◽  
Vol 13 (606) ◽  
pp. eaaz8690
Author(s):  
Nicholas G. Davies ◽  
Stefan Flasche ◽  
Mark Jit ◽  
Katherine E. Atkins

Vaccines against bacterial pathogens can protect recipients from becoming infected with potentially antibiotic-resistant pathogens. However, by altering the selective balance between antibiotic-sensitive and antibiotic-resistant bacterial strains, vaccines may also suppress—or spread—antibiotic resistance among unvaccinated individuals. Predicting the outcome of vaccination requires knowing what drives selection for drug-resistant bacterial pathogens and what maintains the circulation of both antibiotic-sensitive and antibiotic-resistant strains of bacteria. To address this question, we used mathematical modeling and data from 2007 on penicillin consumption and penicillin nonsusceptibility in Streptococcus pneumoniae (pneumococcus) invasive isolates from 27 European countries. We show that the frequency of penicillin resistance in S. pneumoniae can be explained by between-host diversity in antibiotic use, heritable diversity in pneumococcal carriage duration, or frequency-dependent selection brought about by within-host competition between antibiotic-resistant and antibiotic-sensitive S. pneumoniae strains. We used our calibrated models to predict the impact of non–serotype-specific pneumococcal vaccination upon the prevalence of S. pneumoniae carriage, incidence of disease, and frequency of S. pneumoniae antibiotic resistance. We found that the relative strength and directionality of competition between drug-resistant and drug-sensitive pneumococcal strains was the most important determinant of whether vaccination would promote, inhibit, or have little effect upon the evolution of antibiotic resistance. Last, we show that country-specific differences in pathogen transmission substantially altered the predicted impact of vaccination, highlighting that policies for managing antibiotic resistance with vaccines must be tailored to a specific pathogen and setting.

2019 ◽  
Author(s):  
Nicholas G. Davies ◽  
Stefan Flasche ◽  
Mark Jit ◽  
Katherine E. Atkins

Bacterial vaccines can protect recipients from contracting potentially antibiotic-resistant infections. But by altering the selective balance between sensitive and resistant strains, vaccines may also help suppress—or spread—antibiotic resistance among unvaccinated individuals. Predicting the outcome requires knowing the drivers of resistance evolution. Using mathematical modelling, we identify competition and diversity as key mediators of resistance evolution. Specifically, we show that the frequency of penicillin resistance in Streptococcus pneumoniae (pneumococcus) across 27 European countries can be explained by between-host diversity in antibiotic use, heritable diversity in pneumococcal carriage duration, or within-host competition. We use our calibrated model to predict the impact of universal pneumococcal vaccination upon the prevalence of carriage, incidence of disease, and frequency of resistance for S. pneumoniae. The relative strength and directionality of competition between resistant and sensitive pneumococcal strains determines whether vaccination promotes, inhibits, or has little effect on the evolution of antibiotic resistance. Finally, we find that differences in overall bacterial transmission and carriage alter predictions, suggesting that evidence-based policies for managing resistance with vaccines must be tailored to both pathogen and setting.One sentence summaryCompetition and diversity are key to antibiotic resistance evolution and determine whether vaccines will prevent or increase resistant infections.


2020 ◽  
Vol 22 (5) ◽  
pp. 1110-1124 ◽  
Author(s):  
Colin J. Cunningham ◽  
Maria S. Kuyukina ◽  
Irena B. Ivshina ◽  
Alexandr I. Konev ◽  
Tatyana A. Peshkur ◽  
...  

The problems associated with potential risks of antibiotic resistance spreading during bioremediation of oil-contaminated soil are discussed. Careful selection of bacterial strains and pretreatment of organic wastes used as fertilizers are suggested.


2020 ◽  
Vol 41 (04) ◽  
pp. 455-469 ◽  
Author(s):  
Charles Feldman ◽  
Ronald Anderson

AbstractWith the notable exceptions of the United States and Canada in particular, the global burden of disease in adults due to invasive infection with the dangerous respiratory, bacterial pathogen, Streptococcus pneumoniae (pneumococcus) remains. This situation prevails despite the major successes of inclusion of polysaccharide conjugate vaccines (PCVs) in many national childhood immunization programs and associated herd protection in adults, as well as the availability of effective antimicrobial agents. Accurate assessment of the geographic variations in the prevalence of invasive pneumococcal disease (IPD) has, however, been somewhat impeded by the limitations imposed on the acquisition of reliable epidemiological data due to reliance on often insensitive, laboratory-based, pathogen identification procedures. This, in turn, may result in underestimation of the true burden of IPD and represents a primary focus of this review. Other priority topics include the role of PCVs in the changing epidemiology of IPD in adults worldwide, smoking as a risk factor not only in respect of increasing susceptibility for development of IPD, but also in promoting pneumococcal antibiotic resistance. The theme of pneumococcal antibiotic resistance has been expanded to include mechanisms of resistance to commonly used classes of antibiotics, specifically β-lactams, macrolides and fluoroquinolones, and, perhaps somewhat contentiously, the impact of resistance on treatment outcome. Finally, but no less importantly, the role of persistent antigenemia as a driver of a chronic, subclinical, systemic proinflammatory/procoagulant phenotype that may underpin the long-term sequelae and premature mortality of those adults who have recovered from an episode of IPD, is considered.


2019 ◽  
Vol 25 (16) ◽  
pp. 1861-1865 ◽  
Author(s):  
Naira Sahakyan ◽  
Margarit Petrosyan ◽  
Armen Trchounian

Overcoming the antibiotic resistance is nowadays a challenge. There is still no clear strategy to combat this problem. Therefore, the urgent need to find new sources of antibacterial agents exists. According to some literature, substances of plant origin are able to overcome bacterial resistance against antibiotics. Alkanna species plants are among the valuable producers of these metabolites. But there is a problem of obtaining the standardized product. So, this review is focused on the discussion of the possibilities of biotechnological production of antimicrobial agents from Alkanna genus species against some microorganisms including antibiotic resistant bacterial strains.


2018 ◽  
Author(s):  
Alita R. Burmeister ◽  
Rose G. Bender ◽  
Abigail Fortier ◽  
Adam J. Lessing ◽  
Benjamin K. Chan ◽  
...  

AbstractBacterial pathogens are increasingly evolving drug resistance under natural selection from antibiotics in medicine, agriculture, and nature. Meanwhile, bacteria ubiquitously encounter bacteriophages and can rapidly evolve phage resistance. However, the role of phages in interacting with drug-resistant and drug-sensitive bacteria remains unclear. To gain insight into such relationships, we screened for and characterized phages that rely on the multi-drug efflux pump genetolC. First, we screened a collection of 33 environmental and commercialEscherichia coliphages for their ability to infect cells that lackedtolC. Our screen revealed two phages that had reduced efficiency of plating (EOP) on thetolCknockout compared to wild type. We further characterized these phages with bacterial growth curves, transmission electron microscopy, and analysis of phage-resistant mutants. Phage U136B is a curly-tailed virus in familySiphoviridaewith no ability to infect atolCknockout, suggesting TolC is the U136B receptor. Phage 132 is a contractile-tailed virus in familyMyoviridaewith reduced EOP on cells lackingompFand its positive regulatorstolCandompR. U136B and 132 differentially effect bacterial growth and lysis, and U136B-resistant mutants contain mutations of thetolCgene. Together, these results show that thetolCgene involved in drug resistance can modify bacteria-phage interactions in multiple ways, altering bacterial lysis and selection. These new phages offer utility for studying evolution, tradeoffs, and infection mechanisms.ImportanceBacteria face strong selection by antibiotics in medicine and agriculture, resulting in increasing levels of drug resistance among bacterial pathogens. Slowing this process will require an understanding of the environmental contexts in which drug resistance evolutionarily increases or decreases. In this study, we investigate two newly-isolated bacteriophages that rely on a bacterial antibiotic resistance gene. These bacteriophages vary in their interactions with drug-resistant bacteria, with one of the phages selecting for phage-resistant mutants that have mutations in the antibiotic resistance gene. Further study of these new phages will be useful to understanding evolutionary tradeoffs and how phages might be applied in natural settings to reverse the problem of drug resistance.


2021 ◽  
pp. 111-116
Author(s):  
Thomas E. Schindler

This chapter reviews how bacterial sex explains the rapid emergence of superbugs that are resistant to multiple antibiotics, the so-called MDR pathogens. Millions of years before humans evolved, bacteria invented antibiotics and the defensive molecules that make some bacteria resistant to an antibiotic. Therefore, antibiotic resistant genes pre-exist in many bacterial strains, literally lying in wait to emerge in superbugs. In postwar Japan, bacteriologists discovered the first MDR pathogens during dysentery outbreaks. Researchers demonstrated that the genes for resistance to several antibiotics were transferred by bacterial sex—from normal flora to the dysentery pathogens—all together and “at one stroke.” Methicillin was intentionally designed to treat penicillin-resistant infections. Only three years after its introduction of, hospitals began to find methicillin-resistant Staphylococcus aureus (MRSA). Gerard Wright coined the term resistome to signify “the global collection of resistance genes that have been readily available to pathogens for millennia.”


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