University of Tübingen: From harmless skin bacteria to the dreaded infectious agent
The bacterium Staphylococcus epidermidis occurs mostly as a harmless species on human skin and in the nose. However, some strains can cause difficult-to-treat infections in catheters, artificial joints, and heart valves, or in the bloodstream. They are also often resistant to the particularly effective antibiotic methicillin and are among the dreaded hospital germs. How dangerous infectious agents could suddenly develop from harmless skin germs was largely unclear.
An international research team has now discovered what distinguishes the peaceful roommates among the S. epidermidis bacteria from many of the dangerous invaders. In many of the latter, the scientists identified a new gene cluster that helps the bacteria to create additional structures in the cell wall. This allows the staphylococci to attach themselves more easily to human host cells in the bloodstream; as a result, they become pathogens. It is possible that methicillin resistance can also be spread via these cell wall structures and, for example, transferred from Staphylococcus epidermidis to the even more dangerous sister species Staphylococcus aureus .
The study was led by researchers from the Cluster of Excellence “Control of Microorganisms to Fight Infections” (CMFI) at the University of Tübingen and the German Center for Infection Research (DZIF) in cooperation with universities in Copenhagen, Hamburg, Shanghai and Hanover and the German Center for Lung Research (DZL) in Borstel and published in the journal Nature Microbiology .
The structure makes the difference
The cell wall of staphylococci – like other gram-positive bacteria – consists to a large extent of teichonic acids. They protrude outwards like a chain and are known in species-specific variants with different chemical structures. “During our investigations, we found that many pathogenic strains of S. epidermidis have an additional gene cluster that contains the information for the production of the wall pondoic acids that are actually typical for S. aureus ,” reports the researcher Xin Du from the CMFI Cluster of Excellence and the DZIF. Experiments would have shown that S. epidermidis bacteria with the typical wall teichoic acid alone are less invasive and colonize skin and mucous membrane surfaces. Come the forAdding wall teichonic acid, which is typical for S. aureus , means that they cannot grow as well there and instead penetrate the tissues of their human host more successfully. “At some point some S. epidermidis clones took over the corresponding genes from S. aureus and thus became dangerous pathogens,” says Professor Andreas Peschel from the CMFI Cluster of Excellence and the DZIF.
It has long been known that bacteria can transfer properties to one another via gene transfer. The transfer is done by bacteriophages, viruses that attack bacteria. This usually happens within a species and requires the same surface structures to which the bacteriophages have to bind. “Between S. epidermidis and S. aureus , the different cell wall structures normally prevent gene transfer. But with the S. epidermidis strains, which can also produce the wall pond acid from S. aureus , such a gene exchange is suddenly possible, ”says Peschel. So one could explain how S. epidermidisa resistance to methicillin was transferred to the even more threatening – then methicillin-resistant – S. aureus . However, this needs to be investigated more closely. The new results are an important step towards being able to develop better therapies or vaccinations against dangerous pathogens such as S. epidermidis ST 23, which has been known for around 15 years and belongs to the group of HA-MRSE (healthcare-associated methicillin-resistant S. epidermidis ).