Understanding E. coli biofilms in recurrent UTIs

Escherichia coli (E. coli) is a major bacterial group in the digestive tract, found living with other bacteria, with a range of survival tools at its disposal. One such tool is its ability to create biofilms to colonise surfaces.

    What is a biofilm?

A biofilm is a sticky matrix that covers the top layer of cells, protecting microbes from danger, but also blocking the colonisation of other bacteria that may try to colonise that same area. Many friendly bacteria also develop biofilms, but when it comes to pathogens taking charge with biofilms, it means the blockage of friendly bacteria, and chronic and recurrent infections.

Planktonic bacteria – free-floating bugs – can be easily killed with antimicrobials, but biofilms are not affected by biofilms. This means you may have a urinary tract infection (UTI), treated effectively with antibiotics, but that returns quickly and with only slight or no provocation.

Biofilms ensure a bacterial colony is protected from stressors, biological weapons of other microbes (and animals – us and antibiotics), and our normal immune system functions. These biofilms are almost always polymicrobial, as many bacteria that enjoy the same environments can chime in to make the biofilm stronger. These biofilms are commonly found outside the body as well as inside, on catheters and other medical devices.

     How E. coli makes its biofilms

E. coli have appendages that allow them to finely tune their activities to ensure a mature biofilm is developed. Some E. coli are commensal – that is, normally found as part of a microbial community – while others are pathogenic. E. coli has over 250 serotypes, with each with its own characteristics.

E. coli can swim, and resist liquid pressure like the force of a urine stream. These two characteristics make up the main capacity of E. coli to create biofilms. Not all bacteria require motility to create biofilms, but E. coli generally does, along with adhesion capacities.

E. coli’s ability to adhere to cells is dependent on pH, temperature, hydrophobia and ionic forces present. For example teflon and plastic are more likely to be colonised by E. coli than glass or metal.

    The role of mannose in E. coli adhesion

Many E. coli strains have what’s known as fimbriae – tubular filaments made of protein that act as adhesives. Each bacteria may have between 100 and 500 on their surface that provide the bacteria’s sticking power. Mannose, a sugar, is found in the cells that line the urinary tract, and is the thing in the cell that E. coli’s filaments bind to.

This is why D-mannose and cranberry work to either prevent or help treat E. coli-based urinary tract infections, binding to and blocking these filaments so the bacteria is swept out in the urine stream, as it is not attached to the mannose in urinary cells. It’s a biological trick.

     Once attached…

E. coli can then start building its biofilm using adhesins. The biofilm matrix is mostly composed of water, with the rest made up  of polysaccharide polymers, proteins, fats, nutrients and metabolites.

     How to remove a E. coli biofilm

Presently we are working on the UTI ebook and treatment program, however you can go through the Killing BV biofilm busting treatment found in the four-pronged approach, skipping the vaginal treatments and using the oral biofilm busting protocol plus testing your pH and using Aunt Vadge’s UTI Tea. E. coli usually causes alkaline urine, but it actually doesn’t matter if it is alkaline or acidic. You just need the correct herbs for your urinary pH.

The point of treatment is to bust the biofilms while also killing the bacteria in your urinary tract after they are shed from the biofilm, using the herbs. You can also use any of the other non-antibiotic UTI treatments for the bacteria-killing function, or if you have been prescribed antibiotics, you can use them instead of/as well as the non-antibiotic treatment.

     References

  • Beloin C, Roux A, Ghigo J-M. Escherichia coli biofilms. Current Topics in Microbiology and Immunology. 2008;322:249-289.