samedan logo
 
 
 
spacer
home > ebr > autumn 2021 > we are losing our strongest allies against infectious diseases
PUBLICATIONS
European Biopharmaceutical Review

We Are Losing Our Strongest Allies Against Infectious Diseases

Antibiotics are marvellous weapons against infectious diseases. 100 years ago, severe bacterial infections would likely cause death due to lack of effective treatments. Only with the advance of sulfonamides in the 1930s and the discovery of different classes of antibiotics – most prominently, betalactams, tetracyclines, and aminoglycosides in the 1940s and 50s – could clinicians prevent people from dying of systemic bacterial infections. However, shortly after their introduction, pathogenic strains developed antimicrobial resistance (AMR) and limited treatment options – creating the need for alternative drugs (1). In the last 50 years, we witnessed a steep decline in the success rate of finding new antibiotics, owing, not least of all, to the lack of financial incentives that exist for other human menaces like chronic metabolic diseases or cancer. Today, resistant strains have emerged against every clinical antibiotic, leaving us with limited treatment options against multidrugresistant (MDR) and extensively drug-resistant (XDR) strains, or even with no treatment options at all for pan-resistant strains. This trend is leading us into a post-antibiotic era threatening up to 10 million annual deaths and a GDP economic loss of $100 trillion by 2050 (2).

Underlying Mechanisms for AMR

Before Sir Alexander Fleming discovered penicillin, bacteria themselves have been widely using antibiotics in their competition for resources. Consequently, AMR genes have always been present in the environment. AMR can be based on de novo genetic mutations or the acquisition of resistant genes through horizontal gene transfer from bacteria of the same or different species. Antibiotic resistance mechanisms involve enzymes that inactivate the drug or involve efflux pumps that expel the drug from the cell. Other mechanisms are based on changes in membrane permeability, for example, due to loss of porins. Often, point mutations or single nucleotide polymorphisms (SNPs) suffice to confer resistance by interfering with the antibiotic target recognition or upregulate efflux pump gene expression.

Read full article from PDF >>

Rate this article You must be a member of the site to make a vote.  
Average rating:
0
     

There are no comments in regards to this article.

spacer
Alexander Sturm PhD is the Senior Scientist at Resistell AG. Alex was a Research Fellow at the Broad Institute of MIT and Harvard and Massachusetts General Hospital in Boston, Massachusetts, US. Here he worked on the metabolism of non-growing M. tuberculosis and its impact on antibiotic tolerance. Before, at his time at Columbia University in New York, US, he focused on cellular dormancy in spore-forming bacteria and population-level mechanisms to exit dormancy. Alex is a co-recipient of the Broad Institute’s Excellence Award and its TB Gift Innovation Award. He has received fellowships from European Molecular Biology Organization and the German Research Fund. He obtained his PhD from ETH Zurich, Switzerland, on his work on heterogeneous gene expression of Salmonella virulence factors.
spacer
Alexander Sturm PhD
spacer
spacer
Print this page
Send to a friend
Privacy statement
News and Press Releases

Clinical Researcher of the Year - The Americas 2021 winners announced

The winners of the 2021 Clinical Researcher of the Years – The Americas competition have been announced, with the exceptional talent of clinical researchers across the Americas recognised during a live virtual awards ceremony.
More info >>

White Papers
 

 

 

©2000-2011 Samedan Ltd.
Add to favourites

Print this page

Send to a friend
Privacy statement