Brain Inflammation Flowing from Post-Treatment Lyme Disease Syndrome?

In our feature article, within edition 227 of BC Disease News (here), we focused on Lyme disease as an occupational risk most likely to affect workers in agriculture. Infection is typically transmitted when Borrelia burgdorferi bacteria is passed from ticks (host) to humans, i.e. through tick bites.

Since 2000, the number of Lyme disease cases in England and Wales have increased in an upward trend. In 2017, there were around 1,500 laboratory confirmed cases of Lyme disease.[1]

Figure: Number of confirmed cases of Lyme disease in England and Wales

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(Source: Parliamentary Office of Science and Technology)

Individuals who demonstrate longer-term symptoms of Lyme disease infection, such as persisting months of fatigue, pain and aching, are labelled sufferers of ‘post-treatment Lyme disease syndrome’ (PTLDS). This is a medically acknowledged condition, which could also be indicative of chronic fatigue syndrome or fibromyalgia.

PTLDS is not to be confused with ‘chronic Lyme disease’ (CLD), the term given to those who report symptoms of Lyme disease illness without any recorded incidence of Borrelia burgdorferi infection. Clinicians have argued that PTLDS should be distinguished from CLD, as CLD is not medically recognised.[2]

Earlier this month, a small study, published in the Journal of Neuroinflammation,[3] verified that PTLDS patients suffer from brain inflammation. This may explain why sufferers report ‘long-term fatigue, pain, sleep disruption and "brain fog"’.[4]

In this study, the participants underwent a positron emission tomography (PET) scan, in which specially labelled molecules (radiotracers) bind to translocator proteins (TSPO). TSPO are released by immune cells in the brain (microglia and astrocytes) when brain inflammation is present.

Therefore, PET scans can visualise the activation of TSPO and, in theory, illustrate evidence of brain inflammation.

Radiotracer levels were elevated in all 12 of the PTLDS patients, i.e. tested positive for brain inflammation.

What is more, the researchers found that PTLDS patients had significantly higher levels of TSPO, compared with the group of 19 control patients and, contrary to their hypothesis, neuroinflammation was widespread. None of the 8 brain regions tested was more vulnerable than the others.

Ultimately, the study disproved allegations that PTLDS symptoms are ‘psychosomatic or related to depression or anxiety’. Further, it suggests that drugs, designed to reduce neuroinflammation, may be able to treat PTLDS.

 

[1] Common animal associated infections quarterly report (England and Wales): fourth quarter 2017. Public Health England. Health Protection Report Volume 12 Number 5, 9 February 2018. https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/680710/hpr0518_zoos.pdf (Accessed 2 March 2018)

[2] ‘Post-Treatment Lyme Disease Syndrome’ (21 December 2018 CDC) <https://www.cdc.gov/lyme/postlds/index.html> accessed 22 February 2019.

[3] Jennifer M. Coughlin et al. Imaging glial activation in patients with post-treatment Lyme disease symptoms: a pilot study using [11C]DPA-713 PET, Journal of Neuroinflammation (2018). <DOI: 10.1186/s12974-018-1381-4> accessed 22 February 2019.

[4] Johns Hopkins University School of Medicine, ‘New scan technique reveals brain inflammation associated with post-treatment Lyme disease syndrome’ (5 February 2019 Medical Xpress) <https://medicalxpress.com/news/2019-02-scan-technique-reveals-brain-inflammation.html> accessed 22 February 2019.