As scientists delve deeper into the actual biology of Borrelia burgdorferi, rather than just treating the symptoms it causes, they’ve begun to make discoveries with exciting implications for Lyme Disease treatment. One new finding is that the bacterium seems to possess genes for something called the “efflux pump effect.”

If you’re wondering “What the heck is that?” right about now, you’re not alone; the efflux pump effect, or EPE, is a subtle but powerful effect known mostly to medical specialists. But it may help explain why Borrelia can fight off some of the most potent antibiotics… therefore offering hints of how we can eradicate it.

The EPE Explained

In microbiology, the EPE (a.k.a. active efflux) is the term used for a microbe’s ability to quickly move toxic materials out of the cell before those materials can take full effect. Think of the efflux pump as a microscopic sump pump, because that’s exactly what it is.

Antibiotics are toxic to bacteria; ergo, in those bugs that have the appropriate genes, the EPE moves them out of the cell before they can build to sufficient strength to kill the cell.

Borrelia burgdorferi was the third microbial genome ever sequenced (just after Haemophilus influenzae and Mycoplasma genitalium, if you were wondering). It wasn’t long before researchers found the genetic coding for the same efflux pump genes they already knew from the infamous E. coli bacterium.

The Upshot of the EPE

Essentially, efflux pumps create antibiotic resistance in bacteria; not just in Borrelia, but in many other species as well. This is why many antibiotics just stop working, forcing us to try new ones. The effect may contribute to the evolution of so-called “superbugs” that can’t be handled by traditional treatment.

Apparently, the Lyme Disease spirochete just happens to be especially efficient with its efflux pumps; hence the difficulty in stamping it out with standard treatment. The EPE can eject even the tougher, more powerful antibiotics like doxycycline and tetracycline.

The drugs do inhibit the infection, but can’t wipe it out. What we need is an antibiotic that can stop the EPE cold, at least long enough to kill all the spirochetes in a host’s body. We don’t have such a drug yet, but researchers are on the right track.

Enter Tigecycline

Tigecycline New Hope for Lyme Disease Treatment

Tigecycline inhibits the efflux pump effect, so it's not ejected from the cells before it can build to effective levels for lyme disease treatment.

The FDA recently approved a new member of the tetracycline family, tigecycline, for use against infections of the skin and abdominal organs. Tigecycline inhibits the EPE, so it’s not ejected from the cells before it can build to effective levels. Initially, it held great promise for treating LD, especially the most chronic form.

A recent mouse study, however, reveals that even after heavy tigecycline treatment, Borrelia spirochetes can survive within the joints and other hard-to-reach reservoirs — though they do appear to be inactivated, at least temporarily. Whether these findings translate to affected humans remains to be seen.

The Point Is…

The initial tigecycline results may be disappointing, but they do offer hope for people who suffer from LD. Human trials may prove that it works effectively for us; after all, body chemistries vary from species to species, and mice aren’t exactly the perfect experimental model for extrapolating results to humans.

Even if it’s not 100% effective, tigecycline may offer temporary relief for LD sufferers. While this remains to be seen, at the very least our understanding of the EPE, and how it works in Borrelia burgdorferi, offers possibilities for the development of new Lyme Disease treatment protocols in the future.