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Researchers discover that leftover bacterial cell wall fragments may trigger chronic inflammation in some patients, offering new hope for better PTLD treatments
Lyme disease is caused by a bacteria called Borrelia burgdorferi, which is passed to humans through tick bites. When caught early, Lyme disease is usually treated with antibiotics like penicillin or amoxicillin. But for some people, the symptoms don’t go away completely — even after successful treatment. These lingering symptoms can include extreme tiredness, trouble thinking clearly, body aches, and joint pain.
This condition is called Post-Treatment Lyme Disease (PTLD), and it’s more common than many think. A 2022 study found that 14% of people treated early for Lyme still developed PTLD. Doctors have been puzzled by what causes this condition — and how to treat it — since it doesn’t always seem linked to an active infection.
Now, researchers at Northwestern University may have figured out what’s happening. They believe the immune system is reacting to leftover pieces of the Lyme bacteria, even though the bacteria itself is gone. These bits come from the cell wall of the bacteria, which breaks apart during treatment but doesn’t fully leave the body.
Dr. Brandon Jutras, a microbiologist who led the research, says the immune system could be overreacting to these leftovers, causing ongoing inflammation. This idea is similar to one theory behind long COVID-19, where parts of the virus remain in the body and keep the immune system on high alert.
At the center of this discovery is a molecule called peptidoglycan, which forms the outer shell or “skeleton” of most bacteria. It’s a common target for antibiotics, including penicillin. Normally, peptidoglycan is broken down and removed from the body fairly quickly. But in the case of Lyme disease, it’s different.
Jutras and his team found that Lyme bacteria have a unique type of peptidoglycan. It’s chemically different from what’s found in other bacteria, partly because it absorbs certain sugars from ticks — the insect that spreads Lyme disease. This special peptidoglycan is harder for the body to get rid of, and often ends up collecting in the liver or joints, where it can cause trouble for weeks or even months after treatment.
One common sign of PTLD is Lyme arthritis, where joints (especially the knees) become swollen and painful. When scientists studied fluid from swollen joints in Lyme patients, they found traces of Lyme peptidoglycan, even long after the bacteria had been killed by antibiotics.
What’s even more interesting is that some patients don’t improve with more antibiotics — but they do get better when given drugs that calm the immune system, like anti-inflammatory or anti-rheumatic medications. This suggests that what’s making them sick isn’t live bacteria, but rather their body’s ongoing response to the leftover molecules.
Jutras believes that individual genetics might play a role. Some people’s immune systems react more strongly to the lingering molecules than others, which might explain why some people develop PTLD while others don’t.
This discovery is exciting because it could lead to better testing and treatments. Instead of focusing on killing bacteria that are no longer there, doctors might be able to target the inflammatory molecules themselves. Researchers are already working on ways to remove the peptidoglycan from the body, including using monoclonal antibodies — lab-made molecules that can seek out and destroy specific targets.
The study was supported by several major organizations, including the National Institutes of Health and the Department of Defense. It will be published in Science Translational Medicine on April 23.
This breakthrough could offer real hope to people living with the frustrating and painful symptoms of PTLD, by shifting the focus from fighting infection to calming the body’s response.