A Distinct Microbiome Signature in Posttreatment Lyme Disease Patients, 2020, Morrissette et al

Andy

Retired committee member
Lyme disease is the most common vector-borne disease in the United States, with an estimated incidence of 300,000 infections annually. Antibiotic intervention cures Lyme disease in the majority of cases; however, 10 to 20% of patients develop posttreatment Lyme disease syndrome (PTLDS), a debilitating condition characterized by chronic fatigue, pain, and cognitive difficulties. The underlying mechanism responsible for PTLDS symptoms, as well as a reliable diagnostic tool, has remained elusive. We reasoned that the gut microbiome may play an important role in PTLDS given that the symptoms overlap considerably with conditions in which a dysbiotic microbiome has been observed, including mood, cognition, and autoimmune disorders. Analysis of sequencing data from a rigorously curated cohort of patients with PTLDS revealed a gut microbiome signature distinct from that of healthy control subjects, as well as from that of intensive care unit (ICU) patients. Notably, microbiome sequencing data alone were indicative of PTLDS, which presents a potential, novel diagnostic tool for PTLDS.

IMPORTANCE Most patients with acute Lyme disease are cured with antibiotic intervention, but 10 to 20% endure debilitating symptoms such as fatigue, neurological complications, and myalgias after treatment, a condition known as posttreatment Lyme disease syndrome (PTLDS). The etiology of PTLDS is not understood, and objective diagnostic tools are lacking. PTLDS symptoms overlap several diseases in which patients exhibit alterations in their microbiome. We found that patients with PTLDS have a distinct microbiome signature, allowing for an accurate classification of over 80% of analyzed cases. The signature is characterized by an increase in Blautia, a decrease in Bacteroides, and other changes. Importantly, this signature supports the validity of PTLDS and is the first potential biological diagnostic tool for the disease.
Open access, https://mbio.asm.org/content/11/5/e02310-20
 
This is an Aucott product. If memory serves me, isn't he an ex-Infectious-Disease-expert-turned-rheumatologist? Wonder what his emphasis might be.

"...there is no biological method to diagnose PTLDS..."
Sure there is. There are several. At least three are FDA-approved: Conventional ELISA, Western Blot, and C6.

Ok, I'm going stop quoting with that, as it appeared so early on, and the implications to my typing are unsettling.

So, they are examining a downstream effect. Downstream from what? From abx? From cured Lyme and abx, the combination of the two creating a unique signature? From on-going Lyme? From ongoing Lyme combined with abx??

Did they have a control group of acute Lyme patients?

More importantly, by far, did they have a control group of late stage Lyme patients that have received no abx? One with ongoing late stage Lyme that have received abx?

If the answer is no to the last two questions, then the unique signature they may be finding could be from ongoing Lyme infection and abx, not from the PTLDS construct. Until they sort out that rudimentary qualifier, this sort of endeavor in my eyes will have "fallen stillborn from the press"

Edit to add: Thank you @Andy, for posting Lyme stuff, especially in light of the fact that I am usually doing my best to shred what you and others post This does not reflect on my appreciation for you going out of your way to post something that may have no relevance to ME.
 
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