Some infectious bacteria have altered as well as the human gut, they seem to make their own DNA by using chemicals in our urine.
The urinary tract is a hard place for most bacteria to survive. That is why urine is said to be very sterile, although that is not true.
Just like your gut, human urine is home to a community of microbes, called microbiota, and while most of the bacteria that live there are harmless, sometimes a particular species can break down the gut, causing chronic urinary tract infections (UTIs).
Streptococcus agalactiae is a well-known source of UTIs in some people, and new research has now revealed how it can survive in such a friendly environment.
In a healthy human body, urine should be relatively low in the four nucleobases making up the DNA code, which is broken down into nitrogenous fertilizers and excreted.
The sequence of S. agalactiae genome, scientists have now discovered a specific key gene, which allows the bacterium to take advantage of the presence of other compounds in our urine to produce at least one of these centers – guanine – until he survives.
Similar genes have recently been discovered in Escherichia coli (E. coli), the most common culprit of human UTIs.
Usually in the gut or in the blood, E. coli and Streptococcus scavenge for some of the chemicals needed to make DNA, borrowing products like guanine from our own bodies. In the urinary tract, however, these essential building blocks are broken down into uric acid, which means they are less easily detected.
It’s a difficult situation, and it means both E. coli and Streptococcus they need to synthesize their own chemical bases if they are to grow and reproduce.
“It is a survival strategy to colonize the urine, an environment in which many organisms cannot inhabit it,” explained molecular geneticist Matthew Sullivan of Griffith University in Australia.
“It seems to be a common strategy among bacterial species that make up the urine mites.”
In the study, scientists used mice to show how important this special gene, called guaA, is. Collecting Streptococcus series from several individuals, researchers compared normal S. agalactiae infection with a form of the bacterium deficient in guaA.
Microbes that could not form the guanine itself could not colonize a mouse colony to the same extent. The same was discovered when researchers used synthetic human urine.
This suggests that guaA is essential for a Streptococcus infection to the garden, not only in mice but also in us.
When researchers added extra guanine to the urine, even bacterial rays without the metabolic pathways to form guanine on their own were able to survive and thrive, indicating that this base is an essential limiting factor.
The support E. coli, Streptococcus shows key differences in the way it controls guaA genes, but the results appear very similar and give us a new pathway for the treatment of UTIs, which have been increasingly more sustainable than available antibiotics.
Already, methods that target the synthesis of guanine elsewhere in the body have helped to restore other forms of Streptococcus bacteria.
Although not as common as E. coli diseases of the gallbladder, Streptococcus causing about 160,000 UTIs each year in the U.S., and these can be difficult to treat, especially since we know very little about how the disease works.
What’s more, because Streptococcus UTIs often appear in those who are pregnant, elderly, and patients with underlying health conditions such as diabetes, finding safe and effective treatment options is becoming even more difficult.
“Research like this gives us new opportunities to develop alternative therapies in a world with increased antibiotic resistance due to overuse of existing medicine. For example, we could take this path focus in efforts to design new drugs to prevent infection, “Sullivan explained.
“Overall, the study highlights the importance of basic findings that help us see how microorganisms interact with humans.”
The study was published in the Journal of the International Society of Microbial Ecology (ISME).