Some infectious bacteria have adapted so well to the human bladder that they appear to make their own DNA using chemicals in the urine.
The urinary tract is a difficult place for most bacteria to survive. Therefore, it is often said that urine is sterile, although in reality it is not true.
Like your gut, human urine harbors a community of microbes, known as the microbiota, and while most bacteria that live there are harmless, sometimes a particular species can tip the scales and cause painful tract infections. urinary tract (ITU).
Streptococcus agalactiae it is a known source of UTI in some humans, and new research has now revealed how it can survive in such an unfriendly environment.
In a healthy human body, urine must be relatively low at the four nucleobases that make up the DNA code, which break down into nitrogenous compounds and are excreted.
Sequencing of S. agalactiae genome, scientists have now found a key, specialized gene that allows the bacterium to exploit the presence of other compounds in the urine to produce at least one of these bases, guanine, so that it can survive.
Recently, genes similar to Escherichia coli (E. coli), which is the most common offender in human UTIs.
Usually in the intestine or blood, E. coli i Streptococcus look for certain chemicals they need to make DNA, taking products like guanine from our own body. However, in the urinary tract these essential components break down into uric acid, which means they are not as easy to find.
It’s a difficult situation and it means both things E. coli i Streptococcus they have to synthesize their own chemical bases if they want to grow and reproduce.
“It’s basically a survival strategy to colonize urine, an environment where not many organisms can live,” explains molecular geneticist Matthew Sullivan of Griffith University in Australia.
“It seems to be a common strategy among the species of bacteria that make up the urine microbiome.”
In the study, scientists used mice to demonstrate the essentiality of this specialized gene, known as guaA. Collecting Streptococcus strains of several people, the researchers compared a normal S. agalactiae infection with a form of the guaA-deficient bacterium.
Microbes that were unable to create their own guanine were unable to colonize the mouse bladder to the same extent. The same was found when the researchers used synthetic human urine.
This suggests that guaA is essential for Streptococcus infection that takes advantage of the bladder, not only in mice, but also in us.
When the researchers added additional guanine to the urine, even bacterial strains without the metabolic pathways to create guanine alone were able to survive and thrive, suggesting that this basis is an essential limiting factor.
Compared with E. coli, Streptococcus shows key differences in how to control guaA genes, but the results seem quite similar and give us a new way to treat UTIs, which have become increasingly resistant to available antibiotics.
Already techniques aimed at the synthesis of guanine in other parts of the body have 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 ITUs each year in the U.S., and can be difficult to treat, mostly because we don’t know much about how the infection works.
It’s more, because Streptococcus UTIs often appear in pregnant women, the elderly, and patients with underlying health conditions such as diabetes, finding safe and effective treatment options becomes even more complicated.
“Research like this offers us new opportunities to develop alternative treatments in a world with increasing antibiotic resistance due to excessive use of existing drugs. For example, we could guide this path in efforts to design new drugs to prevent infection, ”Sullivan explains.
“Overall, the study sheds light on the importance of the fundamental findings that help us perceive how microorganisms interact with humans.”
The study was published in International Society of Microbial Ecology (ISME) Journal.