Some infectious bacteria have adapted so well to the human bladder that they appear to make their own DNA using chemicals in urine.
The urinary tract is a difficult place for most bacteria to survive. This is why urine is often said to be sterile, although in reality it is not.
Like your gut, human urine is home to a community of microbes, known as the microbiota, and while most of the bacteria that live inside it are harmless, sometimes a particular species can tip the balance and cause infections. painful urinary tract (UTI).
Streptococcus agalactiae it is a known source of urinary tract infections in some humans, and new research has now revealed how it can survive in such a harsh environment.
In a healthy human body, urine should be relatively low in the four nucleic bases that make up the DNA code, which are broken down into nitrogenous compounds and excreted.
Sequencing the S. agalactiae genome, scientists have now found a key specialized gene, which allows bacteria to exploit the presence of other compounds in our urine to produce at least one of these bases, guanine, so that it can survive.
Similar genes have also recently been found in Escherichia coli (E. coli), which is the most common offender of UTIs in humans.
Usually in the gut or blood, E. coli Y Streptococcus look for certain chemicals they need to make DNA, borrowing products like guanine from our own bodies. In the urinary tract, however, these essential building blocks are eventually broken down into uric acid, which means they are not that easy to find.
It’s a tough situation and it means so much E. coli Y Streptococcus they must synthesize their own chemical bases if they want to grow and reproduce.
“It is basically a survival strategy to colonize urine, an environment that many organisms cannot live in,” explains molecular geneticist Matthew Sullivan of Griffith University in Australia.
“It appears to be a common strategy among the species of bacteria that make up the urine microbiome.”
In the study, the scientists used mice to show how essential this specialized gene, known as guaA, really is. Collecting Streptococcus strains from various individuals, the researchers compared a S. agalactiae infection with a guaA-deficient form of the bacteria.
The microbes that could not create their own guanine could not colonize the bladder of the mice to the same extent. The same was found when the researchers used synthetic human urine.
This suggests that guaA is essential for Streptococcus the infection takes root in the bladder, not only in mice, but also in ourselves.
When the researchers added additional guanine to urine, even bacterial strains without the metabolic pathways to create guanine on their own were able to survive and thrive, suggesting that this base is an essential limiting factor.
Compared to E. coli, Streptococcus shows key differences in the way it controls the guaA genes, but the results seem quite similar and provide us with a new way to treat urinary tract infections, which have become increasingly resistant to available antibiotics.
Techniques that target the synthesis of guanine in other parts of the body have already helped to overcome other forms of Streptococcus bacteria
Although it is not as common as E. coli bladder infections Streptococcus It causes approximately 160,000 UTIs each year in the US, and these can be difficult to treat, especially since we don’t know much about how the infection works.
Also, because Streptococcus UTIs often appear in pregnant women, the elderly, and patients with underlying health conditions like diabetes, so finding safe and effective treatment options becomes even more complicated.
“Research like this provides us with new opportunities to develop alternative treatments in a world with increasing resistance to antibiotics due to the overuse of existing drugs. For example, we could target this path in efforts to design new drugs to prevent infections.” explains Sullivan.
“Overall, the study illuminates the importance of fundamental discoveries that help us understand how microorganisms interact with humans.”
The study was published in the Journal of the International Society for Microbial Ecology (ISME).