Group B streptococcus (GBS) hijacks an endogenous enzyme called hyaluronidase to evade the immune system. The findings, published in mBio, represent a novel mechanism of GBS and may be a potential target for drugs against GBS infection.

"We now know that GBS utilizes the enzyme hyaluronidase to prevent detection from the host during pregnancy. If we can devise ways to block this enzyme from dampening host immune responses, this may enable eradication of GBS," proposes Lakshmi Rajagopal, Ph.D. and lead author.

Uterine bacterial infections, specifically of bacterial species that fall under the GBS, are one of the leading causes of disorders in newborns like pneumonia and meningitis. Most alarmingly, however, GBS is also able to cause preterm births.

Preterm births, or premature births, is the leading cause of deaths of newborns and children under 5 years old; there are around 4 million infant deaths associated with premature birth annually, worldwide.

While most of these cases are in the poorer regions where health care systems are weak, preterm births are also devastating for developed countries costing them billions of dollars annually.

Of the premature birth cases, at least 25 percent are associated with bacterial infection. Specifically, bacteria which fall under GBS are commonly implicated in these infections.

Usually centered on the uterus, the infection typically starts in the cervix sand slowly ascends.

In the uterus, the bacteria can effect physiological responses that devastate the foetus. These reactions include strong immune responses, particularly inflammation; rupture of the membrane surrounding the fetus, and premature uterine contractions.

Around 30 percent of healthy women have vaginal and rectal GBS infections. However, since these mostly do not display symptoms, most of the infections largely go undiagnosed and untreated.

Despite the large number of women infected, much is still unknown about the mechanisms of GBS infection. To remedy this, the research team obtained GBS from women in labor and infected newborns and found that these had higher hyaluronidase activity compared to isolates from healthy women.

To further explore the role of hyaluronidase, the research team used mice models. They found that higher levels and activities of hyaluronidase were associated with more powerful infections, more frequent premature births, and more fetal deaths.

This, they observed, was because hyaluronidase was able to suppress the immune response in the uterus, but not in the placenta or the foetus.

Their findings, the researchers write, imply that GBS is able to use hyaluronidase to hide from the mothers’ immune system.

Because their findings are still preliminary, the researchers propose that more investigation on hyaluronidase and GBS be done.

However, they remain hopeful that their findings will eventually contribute to new approaches in treating GBS infection in pregnant women. MIMS