It's not every day that a Lyme disease case goes chronic. However, enough cases occur across the globe every year for experts to understand that it can ruin lives indefinitely. Now new research has revealed that hardy and well-hidden bacterium can keep the disease going, and that a well-known cancer treatment, of all things, could deliver a finishing blow.

That's at least according to a study recently published in the journal Antimicrobial Agents and Chemotherapy which details how the bacteria behind persistent Lyme arthritis - a major and often crippling consequence of chronic Lyme disease - can act differently than your run-of-the-mill Borrelia burgdorferi.

Traditionally, B. burgdorferi finds its way into a human host after an unnoticed tick is left to feed for an extended period of time. Tick saliva, which delivers the bacterium, also helps suppress initial immune system responses, allowing the disease to slip in and buy enough time to establish itself (~24 hr). It's after this time that the bacterium usually rears its ugly head, battling the immune system with sheer numbers as it makes its way to spread from the bloodstream to joints (within a week's time) and even to the brain.

Aside from a notable bulls-eye rash caused by inflammation around an infected bite, a patient may feel exhaustion and sores, but not always. According to researchers, dormant forms of B. burgdorferi called persisters remain hidden even after the disease launches its full frontal assault. In this way, they do not grow and multiply, but are also invisible to the immune system - allowing them to restart the war on a host's body if their brethren lose to contemporary medicine.

To determine just why broad antibiotics aren't eliminating these spy-like pathogens, investigators first tested ADEP4, a compound which they had shown to have the ability to kill persisters of other species. Traditionally, this drug works by simply activating a 'kill switch' that only dormant cells boast, but it appeared to have no effect on Lyme disease's sleeper agents.

"It seemed like the microbe is perfectly protected, and that we had hit a dead end," Kim Lewis, Director of the Antimicrobial Discovery Center at Northeastern University, said in a statement.

However he and his colleagues didn't give up. (Scroll to read on...)

"One clue that followed from analyzing [the dormant Lyme cells'] genome was that important genes responsible for repairing the DNA are missing," Lewis explained.

This revelation alone was enough for Bijaya Sharma, a graduate student and first author of the paper, to be reminded of mitomycin C. This intriguing anti-cancer agent is often used against aggressive tumor formation, as it binds and confounds DNA. In a cell where a means for DNA repair does not exist, Sharma suspected that such an attack could be devastating.

And it turns out she was right.

"A single dose eradicated all cells of the pathogen in a test tube," Lewis recently announced.

Still, it's important to note that this isn't the end-all for Lyme disease. While the cancer treatment proved effective, it is far too aggressive and costly to treat a disease that usually does not kill its patients. Among other things, mitomycin C causes a reduction of white blood cells, leaving patients vulnerable to deadly infection, and can sometimes cause kidney damage if a patient is not closely monitored.

Still, it's a step in the right direction, and one that hikers - with the warm tick season upon them - will be happy to hear.

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