Crop, animal, poultry and fishery production requires the use of antibiotics to keep spoilage and pathogenic bacterial population in check. Their misuse has been a problem ever since the start of the industrial revolution and has contributed to the current scourge of antimicrobial resistance. Each year 700 000 deaths are attributed to ineffective antibiotics.
The issue with antimicrobial resistance
Antibiotic resistant strains of bacteria evolve mainly by inheriting genes through plasmids and transposons. The less discussed, but equally important story, is the strategy used by bacteria to survive the first encounter with an antimicrobial compound when they do not have resistance genes in their arsenal – adaptation.
Physiological resilience as an alternative for resistance
Physiological adaptations occur in small communities of bacteria. In a population, this results in resistant outliers. These include slow growers that do not take up antimicrobial compounds or slime formers that produce a biofilm. Scientists have also discovered giant bacterial cells known as filaments. While regular bacterial cells of some species like E. coli or Salmonella are usually 2 to 4 microns in length (a micron is a millionth of the meter), these microbial filaments can be hundreds of times longer.
These giant bacterial filaments were observed when subjecting cells to stress such as drying, starvation, high concentration of salts, and antimicrobials. Such conditions often are present in a food processing plants, farms or hospitals.
Analysis of these filaments revealed that they were formed due to the synthesis of a protein called QueE. It blocks the machinery responsible for the split between two daughter bacterial cells. The result – cells divided, but did not separated, forming giant bacterial rods of cells clumped together.
The task was to understand why bacterial cells form these giant filaments. Different populations of the bacteria were studied and researchers discovered that over time and with the change of the environment, these filaments can fall apart. This led to the bacterial cells which were part of the filament to be released, increasing the number of free, active bacteria.
Turns out, the filaments served as a repository of cells. In them, bacteria were protected from the environmental stress or antimicrobials, and then released back into the environment. This strategy was themed “The Trojan horse”. Is ensures cells can divide even during exposure to antibiotics. The spike in cell count when the filaments break down, further ensures repopulation of the environment once the stress is removed.
Is there a work around this type of bacterial resilience?
While giant bacterial cells serving as “Trojan horse” sounds ominous, researchers showed that increasing magnesium levels blocks the formation of these giant cells. Another effective method of preventing the development of different types of bacterial adaptations against drugs is always following your doctor’s prescription and finishing the course of antibiotics or sticking the to “user instructions” on the label of your disinfectant.
This blog post, along with the microscopy picture in the middle were submitter by Govindaraj Dev Kumar – a co-author of one of the studies behind this post (article here) and edited by me – Nevena.
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