Some infectious bacteria have adapted so well to the human bladder that they seem to make their own DNA using chemicals in our urine.
The urinary tract is a difficult place for most bacteria to survive. That is why urine is often considered sterile, although this is not true.
Like your gut, human urine is home to a community of microbes, known as a microbiota, and while most bacteria that live inside it are harmless, sometimes a particular species can tip the scale, causing painful infections of the tract. urinary tract (UTI).
Streptococcus agalactiae is a known source of ITUs in some humans, and new research has revealed how it can survive in such a hostile environment.
In a healthy human body, urine must be relatively low in the four nucleobases that make up the DNA code, which are broken down into nitrogenous compounds and excreted.
Sequencing the S. agalactiae genome, scientists have now discovered a key specialized gene, which allows the bacteria to exploit the presence of other compounds in our urine to produce at least one of these bases – guanine – to survive.
Similar genes have also been found recently in Escherichia coli (E. coli), which is the most common aggressor of human UTIs.
Normally, in the intestine or blood, E. coli and Streptococcus they scour 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 ultimately broken down into uric acid, which means they are not so easy to find.
It is a difficult situation and it means so much E. coli and 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 in which few organisms can live,” 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, scientists used mice to show how essential this specialized gene, known as guaA, is. Collecting Streptococcus strains of several individuals, the researchers compared a normal S. agalactiae infection by a water-deficient form of the bacterium.
Microbes that were unable to create their own guanine were unable to colonize the bladder of mice to the same extent. The same thing was found when researchers used synthetic human urine.
This suggests that guaA is essential for a Streptococcus infection to spread in the bladder, not only in mice, but also in us.
When the researchers added extra guanine to the urine, even bacterial strains lacking 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 the main differences in the way it controls guaA genes, but the results seem quite similar and give us a new path for the treatment of UTIs, which have become increasingly resistant to available antibiotics.
Already, the techniques that aim at the synthesis of guanine in other parts of the body helped to overcome other forms of Streptococcus bacteria.
Although it is not as common as E. coli bladder infections, Streptococcus it causes about 160,000 UTIs a year in the United States and can be difficult to treat, especially since we don’t know much about how the infection works.
Furthermore, because Streptococcus UTIs often appear in pregnant women, the elderly, and patients with underlying health problems, such as diabetes, and finding safe and effective treatment options becomes even more complicated.
“Research like this gives us 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 direct this path in efforts to develop new drugs to prevent infection, ”explains Sullivan.
“Overall, the study sheds light on the importance of fundamental discoveries that help us understand how microorganisms interact with humans.”
The study was published in Journal of the International Society for Microbial Ecology (ISME).