- For some people with Lyme disease, symptoms extend well beyond “successful” treatment with antibiotics.
- A new study finds that dead, left-behind bits of the bacteria that cause Lyme disease may be the culprit.
- The research shows that these unviable fragments cause even more neurological and musculoskeletal inflammation than the live bacteria.
- It is hoped that future treatment can neutralize or clear out these lingering fragments.
A 2-to-4-week regimen of oral antibiotics cures Lyme disease for most people. However, for some, the symptoms linger for months. Among these symptoms are cognitive dysfunction — difficulty thinking — and musculoskeletal pain.
A new study from researchers at Tulane University, in New Orleans, has discovered what may be the reason.
After antibiotics have treated the bacteria responsible for Lyme disease, dead fragments are left behind, and these cause inflammation in the central and peripheral nervous systems.
Lead study author Dr. Geetha Parthasarathy, an assistant professor of microbiology and immunology at Tulane University’s National Primate Research Center, explains:
“As neuroinflammation is the basis of many neurological disorders, lingering inflammation in the brain due to these unresolved fragments could cause long-term health consequences.”
Dr. Michal Křupka, of Palacký University Olomouc, in Czechia — who was not involved in the study — told Medical News Today, “Excessive activation of the immune system is thought to play a role in this case, rather than the infection itself.”
In an email to MNT, Dr. Parthasarathy wrote:
“In essence, if a live bacterium is like a packed suitcase, then dead bacterial debris is like its contents upended, covering a larger area, stimulating more cells to release more inflammatory mediators.”
The study has been published in Scientific Reports.
Traces of post-treatment Lyme disease syndrome
According to the study, 10–35% of people with Lyme disease eventually develop post-treatment Lyme disease syndrome (PTLDS).
In PET brain scans of people with PTLDS, other researchers have detected signs of glial activation many months after treatment, signifying persistent neuroinflammation. Glial cells are types of brain cells; they play a number of supporting roles for neurons.
The type of bacteria that cause Lyme disease is Borrelia burgdorferi.
For this study, the researchers analyzed the effect of B. burgdorferi detritus in the brains of rhesus macaques who had been exposed to sonicated fragments of the bacteria. Sonication involves using ultrasound vibration to break up cells.
In particular, the team investigated the effects of these fragments in the frontal cortex and dorsal root ganglia of the monkeys.
Surprisingly, glial inflammation in these areas was several times more pronounced than it was in macaques who had been exposed to live B. burgdorferi. Researchers found that it was significantly more prevalent in the frontal cortex than in the dorsal root ganglion.
The researchers demonstrated that B. burgdorferi fragments resulted in the cell death of neurons.
They speculate that bacteria broken down by antibiotics release “multiple ligands, such as lipoproteins, flagellins, DNA, RNA, and others” in higher quantities than live bacteria.
Post-infection havoc
In someone with Lyme disease, B. burgdorferi enter the body through a tick bite. It can cause a characteristic bull’s-eye rash, followed by a headache, a fever, and malaise, after which the bacteria disseminate to other organs.
“Fragments do not have to travel to the brain,” said Dr. Křupka. “It would probably be parts of bacteria that entered the brain during acute neuroinfection, and [which] may persist even after antibiotic treatment. These residues could then cause a chronic inflammatory reaction.”
Dr. Parthasarathy plans further investigation into ineffective clearing out of bacterial fragments. She also intends to explore new anti-inflammatory strategies for B. burgdorferi.
Source: Read Full Article