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Inadequate development of new antibiotics and rising rates of resistance by bacteria to existing antimicrobials are dual forces pushing the world ever closer to a post-antibiotic era. It has been an 80-year war, the battle pitched by bacteria against the chemical warfare designed to knock out infections—and on multiple fronts, bacteria have gained the upper hand. Despite their microscopic size and lack of a brain, they know how to win the resistance war.

A team of researchers at Weill Cornell Medicine in New York and the MRC Centre for Molecular Bacteriology and Infection at Imperial College London has tackled how bacteria became resistant in the first place. They have deconstructed bacterial genetic strategies and other survival tactics, which they posit can pave the way to new types of antibiotics while saving many of the existing ones.

Researchers found the intricacies of antimicrobial resistance. They distinguished between heritable resistance—the acquisition of genes that confer resistance, and another type called phenotypic antimicrobial resistance. The latter refers to a reversible form of drug resistance not attributable to genes.

Drug resistance is one of several defenses against infectious disease that is on the decline. In addition to our immune system, our major defenses against infectious disease are antibiotics, vaccines, sanitation, potable water, sound nutrition and public health infrastructure. All of these are failing in various parts of the world.

One key defense, the use of antibiotics, is beginning to fail worldwide because of the rise of antibiotic resistance, which is threatening to undermine the practice of medicine.

Nowhere in infectious diseases has the fight against resistance been more persistent than in the ongoing battle against tuberculosis, which has become a multi-drug-resistant scourge in many parts of the world despite improvements in drug regimens and medication compliance programs. Phenotypic antimicrobial resistance has been a problem with TB.

Phenotypic antimicrobial resistance can arise under a variety of circumstances, and may sometimes be difficult to distinguish from genetically caused resistance. For example, phenotypic resistance can arise stochastically, which means it develops randomly and has a random distribution pattern.

Microbiologists also refer to this type of resistance as "spontaneous persistence" and "stochastic switching." But there are other causes of phenotypic resistance, which additionally can arise from bacterial exposure to conditions of altered environments, such as oxygen deprivation, acidification, oxidative stress, host immune responses and sub-lethal concentrations of antibiotics. As it turns out, phenotypic antibiotic resistance is more common than genetic resistance.

The new analysis covers years of cumulative data about the nuances of drug resistance, a phenomenon that has proved lethal for countless patients around the world.

The assertion that phenotypic antimicrobial resistance is more common than genetic is justified clinically by the prevalence of phenotypically resistant bacteria in biofilms and the presence of biofilms in many clinical settings.

A biofilm is a thick architectural assemblage of microbial cells that form a shell-like encasement with a layer of slime. The sole biological aim is to protect the bacterial colony inside, allowing it to thrive. Biofilms are most dangerous when they invade human cells shielding bacteria from antibiotics.

Source: Sarah M.Schrader et al. Biology of antimicrobial resistance and approaches to combat it, Science Translational Medicine (2020). DOI: 10.1126/scitranslmed.aaz6992

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