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No, Lyme Disease is not Thousands of Years Old Despite What “Fact Checkers” and Some Dishonest Scientists Say

By: A. W. Finnegan 

It is astounding to me just how inaccurate some of these so-called “fact-checked” articles can be when they write articles claiming to give the “facts” and stand as the arbiter of truth. These writers sometimes know next to nothing about the subject they write about, which is clear to those that do know about it. They jump to erroneous conclusions citing studies that are totally inconclusive and making unscientific claims and the fact checkers repeat it as though it is scientific fact, Lyme disease is one example.  

Recently, I came across an article “fact-checked” from April 2022 “Fact Check: Lyme Disease Was NOT Invented In A Lab In 1975 -- Its Bacteria Is Thousands of Years Old,” [1] by: Marlo Lee writing for Lead Stories, a “fact checking” site that is stamped with approval by Meta (Facebook) and the International Fact-Checking Network (IFCN). The article was about Lyme disease originating from the Plum Island laboratory in 1975, due to Erich Traub’s work there.  

What I agree with in this article, is that Lyme disease was not invented at the Plum Island lab in 1975, it was weaponized long before, in Germany, but Traub conducted tests there with his weaponized strains, but let’s be clear about what we mean by weaponized. The actual spirochete, before it was weaponized, has been around for perhaps millions or billions of years, it was a bird strain of Borrelia called Borrelia anserina,[2] and it is true that it did not originate from Plum Island in 1975, because it had been weaponized in Germany starting in 1939, and it had several developments, but may have been weaponized once more during Traub’s return to the United States after WWII and conducted tests with it on Plum Island.  

However, being weaponized does not mean it was created from scratch, it weaponized the naturally existing Borrelia anserina with naturally existing viruses and lipoproteins so that when complete, it was different from the earlier Borrelia anserina. It had new properties and could infect many new species of animals and humans, due to the methods Erich Traub used in bioengineering, animal passages, and this method has been explained in other articles.  

Lab 257 was correct about Lyme disease and Erich Traub

The article cites an article from 2004 from The New York Times about Michael Christopher Carroll's book Lab 257: The Disturbing Story of the Governments Secret Plum Island Germ Laboratory, to show that a spokeswoman from the Agricultural Research Service (ARS) of the USDA voices no association she knows that Erich Traub had to Plum Island.[2] However, this is wrong, and the ARS official probably knew it was wrong and was saying it out of damage control.

My book, The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare, shows that Traub was employed by the Agricultural Research Service at Plum Island and he was brought there because of the original public law for its construction, Public Law 496, 80th Congress,[3] as a chief scientist for the Agricultural Research Service at the Greenport, Long Island station of the ARS, which is Plum Island, and FBI documents actually confirm this, [4] but fact-checkers haven’t looked at any of these documents. They only bolster the official talking points coming from “authorities” but they don’t actually specialize with expertise about what they write. 


Next, the idea that Lyme disease is thousands of years old is totally unsubstantiated and an unscientific claim. She says in the article, “Scientists in Italy found a 5,300-year-old mummy who had the oldest known case of Lyme disease, according to genetic tests performed after its discovery.” No, the scientists did not find Borrelia burgdorferi, or even Borellia afzelii, nor Borrelia garinii, three species of Borrelia responsible for Lyme disease. They found merely traces of what they thought might be from Borrelia spirochetes, but they said further testing is necessary to confirm it was even Borrelia, but what their published research about it shows us is anything but conclusive: 

While several reads were specific for Borrelia, the 60% coverage still represents an upper boundary as reads may map to other species besides Borrelia. [5]

Furthermore, they failed to point out the incompetence of the Next Generation Sequencing (NGS) technology for Whole Genome Sequencing (WGS), and particularly for Borrelia burgdorferi. It is highlighted in a paper specifically addressing the inadequecy of Whole Genome Sequencing for Borrelia burgdorferi

However, the power of NGS has not yet been fully harnessed for vector-borne and zoonotic disease (VBZ) systems, the majority of globally emerging infectious diseases. [...] This is due to the high ratio of host (the arthropod vector or the reservoir host) to pathogen DNA present in mixed DNA samples [11, 12]. The overwhelming presence of this exogenous DNA (which may also include commensal bacteria, endosymbionts, and environmental microbes) renders shotgun sequencing inefficient and cost-prohibitive.


The agent of the most prevalent vector-borne disease in the US, the Lyme disease bacterium, Borrelia burgdorferi sensu stricto, exemplifies this common hurdle to genomic study for many VBZ systems. [...] Shotgun approaches for WGS of pathogens directly from field samples are inefficient due to the excess of contaminating host DNA present in the samples, which result in very low sequence coverage of the low copy number bacterial genomes present. [6]


The scientists conducting the sequencing on the mummy failed to disclose this fact when they suggested that Lyme disease was present in the mummy. But it was repeated by Live Science and the fact-checker as though it was an absolute fact that the mummy had Lyme disease.  

The fact-checker then goes on to say, “Researchers at Yale School of Medicine found that Borrelia burgdorferi, the bacterium that causes Lyme disease, existed for at least 60,000 years in the northeastern region of the United States.” Here is another instance of reporting something as a fact that was entirely inconclusive and based on a mere guess. The Yale researchers made this conclusion off a totally unsubstantiated theory based on 146 ticks collected from the range of 1984-2013, and by looking at mutation rates of genes and phylogeography. For those who don’t know what that means:  

Phylogeography is the study of the historical processes that may be responsible for the past to present geographic distributions of genealogical lineages. This is accomplished by considering the geographic distribution of individuals in light of genetics, particularly population genetics. 


Past events that can be inferred include population expansion, population bottlenecks, vicariance, dispersal, and migration. Recently developed approaches integrating coalescent theory or the genealogical history of alleles and distributional information can more accurately address the relative roles of these different historical forces in shaping current patterns. [7]


Just to be clear, when something is inferred, it means that it is to “form an opinion or guess that something is true because of the information that you have.” Furthermore, this theory is made without taking into consideration the factors that interfere with this theory, like man-made intervention such as bioengineering.  

Moreover, it is further hampered by limitations to their study, which I would describe as entirely unreliable, due to the fact that they cannot get an accurate picture of each specific sample of Borrelia burgdorferi genes since it is often picking up multiple infections in one sample, and the incompetence is further laid bare:  

One limitation to this study is that phylogenies are inferred from consensus bacterial sequences from each individual tick sample. [...] However, the consensus sequence may alternatively represent a chimeric sequence, a combination of segments of the multiple co-infecting haplotypes. With short-read sequence data used here, we are unable to reconstruct multiple bacterial haplotypes within a single sample. Longer-read sequencing will enable sequencing multiple bacterial genomes from individual tick vectors in the future. [8]

Now, essentially, this means that they cannot accurately read each sample, and at best it is a guess, and keep in mind, the data gathered from each guessed sample are then interpreted as a whole to make yet another guess about its possible evolution through phylogeography. 

Next, the Yale researchers also cite a paper claiming that Lyme disease was found in 2 mouse tissue samples from 1896, [9] but that paper was refuted by Richard Marconi et al., from the NIH Rocky Mountains Laboratory, after pointing out that the set of primers they used for testing were not reliable. [10] In these two mouse tissue samples, they only found tiny fractions of the outer surface protein OspA plasmid which contain material shared with viruses of the poxvirus family. It is also extracellular DNA which changes all the time and assimilates DNA from foreign sources,[11][12] making it totally unscientific to say that it is evidence of a Borrelia burgdorferi infection, and they specifically address this in one of their other papers, explaining that they can find “plasmid DNA (which contains telomeres that are homologous to those of vaccinia virus) in human tissues independent of B. burgdorferi infection. [13] 

I rest my case. I hope this points out for the reader just how the “authority” talking points cannot be trusted regarding this matter, and for pretty much any other. One always has to investigate for oneself. They have been actively trying to cover-up these misdeeds for decades and they were using the scientific community to do it, just as they did with the Lyme Disease diagnostic testing, which the organization TruthCures has so eloquently shown. My book The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare tells the story of Lyme disease and biological warfare, for the first time, and is able to link it to the work of Dr. Erich Traub in Germany starting in 1939 and it had several developments during World War II and it was further weaponized upon his return to American shores to work for the military and USDA through Operation Paperclip.  

[1] Lee, M. (2023, May 15). Fact check: Lyme disease was not invented in a lab in 1975 -- its bacteria is thousands of years old. Lead Stories.

[2] Walker, R L et al. “Shared flagellar epitopes of Borrelia burgdorferi and Borrelia anserina.” Veterinary microbiology vol. 19,4 (1989): 361-71. doi:10.1016/0378-1135(89)90101-6

[3] Congressional Hearing. (1970, January 1). Legislative history, public law 496 - 80th Congress, Chapter 229 - 2D session, S. 2038 : United States, Department of Agriculture, office of the general counsel : Free download, borrow, and streaming. Internet Archive.

[3] Rather, J. (2004, February 15). Heaping more dirt on Plum I. (published 2004). The New York Times. 

[4] National Archives. RG 65 Erich Traub, (Declassified FBI Investigations on the Loyalties of Erich Traub). Federal Bureau of Investigation (FBI): NARA., Doc. # QO1-458431291

[5] Keller, A. et al. New insights into the Tyrolean Iceman’s origin and phenotype as inferred by whole-genome sequencing. Nat. Commun. 3:698 doi: 10.1038/ncomms1701 (2012). 

[6] Carpi, G., Walter, K. S., Bent, S. J., Hoen, A. G., Diuk-Wasser, M., & Caccone, A. (2015). Whole genome capture of vector-borne pathogens from mixed DNA samples: a case study of Borrelia burgdorferi. BMC Genomics, 16(1). doi:10.1186/s12864-015-1634-x

[7] Wikipedia. (2024b, March 12). Phylogeography. Retreived from:

[8] Walter, Katharine S et al. “Genomic insights into the ancient spread of Lyme disease across North America.” Nature ecology & evolution vol. 1,10 (2017): 1569-1576. doi:10.1038/s41559-017-0282-8

[9] Walter, Katharine S et al. “Genomic insights into the ancient spread of Lyme disease across North America.” Nature ecology & evolution vol. 1,10 (2017): 1569-1576. doi:10.1038/s41559-017-0282-8

[10] Marconi, R T et al. “Variability of osp genes and gene products among species of Lyme disease spirochetes.” Infection and immunity vol. 61,6 (1993): 2611-7. doi:10.1128/iai.61.6.2611-2617.1993 

[11] Marconi, R T et al. “Variability of osp genes and gene products among species of Lyme disease spirochetes.” Infection and immunity vol. 61,6 (1993): 2611-7. doi:10.1128/iai.61.6.2611-2617.1993 

[12] Zumstein G, Fuchs R, Hofmann A, Preac-Mursic V, Soutschek E, Wilske B. Genetic polymorphism of the gene encoding the outer surface protein A (OspA) of Borrelia burgdorferi. Med Microbiol Immunol. 1992;181(2):57-70. doi:10.1007/BF00189424 

[13] Persing, DH et al. (1994). Target Imbalance: Disparity of Borrelia burgdorferi Genetic Material in  Synovial Fluid from Lyme Arthritis Patients. Journal of Infectious Diseases, 169(3), 668–672. doi:10.1093/infdis/169.3.668 



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