Lyme disease bioweapon theory of John Loftus and Adam Finnegan (part 2) - sars2.net

First published 2026-03-29 UTC, last modified 2026-03-29 UTC

This part is about Adam Finnegan, but part 1 covers John Loftus, Mike Carroll, and other topics: lyme.html.

Contents

The Sleeper Agent

Counterintelligence agent Dan Benjamin

Anne and Dan Benjamin were 2 of the 5 people Finnegan mentioned by name in the dedication of his book: [https://play.google.com/books/reader?id=aTKdEQAAQBAJ&pg=GBS.PT5]

I want to dedicate this book to all the injured and sick people in the world, afflicted and affected by these horrific diseases, who struggle to cope and know the 'why' behind their suffering. Why they are brushed aside and neglected by physicians and the medical establishment? Why they suffer and what is the cause of it? Why they can't seem to recover no matter what they do? Why they have no answers and no official recognition of their suffering and most of all, a very real disease.

I dedicate this book to all Lyme and chronic disease activists who genuinely sought and fought for change in the hopes of dealing with this terrible nine-headed hydra of immune tolerance and all of its classic manifestations and co-infecting agents. I thank the girls who worked in TruthCures and those who began to shine light on immune tolerance. A very special **thank you to Jena Blair and Laura Hovind** for teaching me the basics of immune tolerance when I was coming to the realization of what my disease was, and through this were the keys that opened so many other doors critical to the rest of the story.

I want to dedicate this book to John Loftus, for having the compassion to reveal these dark secrets festering underneath Western civilization with many victims, unwarned and unprepared for the steady rise and proliferation of mystery diseases, chronic diseases that evade a diagnosis or admission of illness. This was a courageous and honorable deed that allowed for this entire book to be written. Without John Loftus, none of the keys that unlock so many other doors in the history of biological warfare and bioterrorism, would have been opened. We thank you for your courage, care, and compassion to do what is right at considerable risk, but nonetheless heroic.

Finally, I dedicate this book to Anne and Dan Benjamin, for their work and intelligence on Dr. Traub, with their desire to have this case on war criminals in Paperclip to be 're-opened.' A line of life work I never would have predicted myself to have taken on, the arduous, meticulous work of pasting together the history of some truly sinister intentions they initially took on and discovered. Though I never met them, this book carried on the torch of Light they shined in dark places with their brilliance to achieve and uncover some of the unspeakable evils that lurk in this world.

Dan Benjamin wasn't mentioned in The Belarus Secret, but there were two references to him in the new introduction Loftus wrote for America's Nazi Secret. First Loftus wrote: "He was the Justice Department lawyer who let free all the American corporate executives who had stayed in Germany to help their Nazi clients. These businessmen had literally given aid and comfort to the enemy during the war. All the striped-suit traitors were held in a joint prison camp code named Ashcan/Dustbin." [https://www.google.com/books?id=YzqdEQAAQBAJ&pg=PP31] Which was followed by this footnote: "My source on this was Dan Benjamin of the US Army Counter-Intelligence Corps. He had worked up many of the treason investigations and was appalled when the Justice Department let them all go free. Dan introduced me to a select circle of intelligence officials who explained to me how the Justice Department really worked."

Then Loftus wrote: "Because of a lack of witnesses, and dwindling resources, Rockler had been finally forced to drop the investigation against Herman Abs and Deutsche Bank. The very next day Abs was appointed economic adviser to the British Zone of Occupied Germany. All of the British residents of Ashcan/Dustbin were quietly released. Several members of the British Royal Family had Nazi dossiers that were quietly returned by American intelligence to the British Secret Service." Which was followed by this footnote: "According to Dan Benjamin, US intelligence had discovered voluminous correspondence between a member of the British royal family and the SS. The British intelligence officer sent to retrieve the dossier was rewarded by appointment as the Queen's personal art advisor. He later confessed to having been a spy for the Russian intelligence service. He was, of course, never prosecuted, in order to protect the Queen."

Grok said that Ashcan and Dustbin did not form a "joint camp", even though Dustbin was sometimes described as the British counterpart to Ashcan, and Grok said:

[...]

Historical records confirm Ashcan and Dustbin existed and held Nazis/industrialists/scientists, but no mainstream sources support Loftus's assertions of American "striped-suit traitors" or British royal Nazi correspondences being processed there. Some references to Ashcan/Dustbin appear in Loftus-related discussions (e.g., interviews, forums quoting his books), but these echo his narrative rather than independently verify it. Dan Benjamin (CIC/treason investigations) does not appear in verifiable WWII CIC histories tied to these claims.

The combined term "Ashcan/Dustbin" appears to mainly be used by Loftus. There was only one hit on Google Search for "Dan Benjamin" "Ashcan" "Dustbin", which was Loftus's book. His book was similarly the only hit for "Counter Intelligence Corps" "Dan Benjamin".

I wasn't able to determine if Dan Benjamin was a real person or not, but Grok said: "'Dan Benjamin' as a CIC veteran appears to be a figure cited exclusively by Loftus, without external confirmation from military archives, declassified files, or scholarly works on US counterintelligence. This aligns with critiques of Loftus's books as relying on unverified insider sources for sensational claims."

In 2021 Loftus wrote: [https://amimagazine.org/2021/01/06/the-greatest-spy-scandal-in-the-world/]

It seemed to me that the British government was almost encouraging these Communist spies to escape rather than face a public trial in England. "They were," said Dan Benjamin, a senior agent of the US Army's Counterintelligence Corps (CIC). His wife, Anne, nodded in agreement. She had met her husband in Germany, where she had been assigned by the SIS to run the intelligence archives for former Nazi scientists wanted for recruitment by Field Intelligence Agency Technical, the British version of Operation Paperclip.

Anne and Dan soon realized that there must be a double agent inside the SIS who was sending the cream of the Nazi rocket scientists to Moscow, while the Americans got useless Nazi bureaucrats like Wernher von Braun or scientists who were Nazi war criminals like Albertus Strughold and Arthur Rudolf. The Russians put Sputnik into orbit, while our rockets kept blowing up on the launching pad. After MacLean and Philby defected to Moscow, the American government grudgingly recognized that Dan and Anne might be on to something.

SIS refers to MI6, which is also known as the Special Intelligence Service.

In his book Finnegan wrote: "Just after WWII, the revelations of Igor Gouzenko exposed massive spy rings operating in Britain, Canada, and the United States.[13] As a result, this eventually led to the discovery of Traub's handler, the one who helped him get cleared for Operation Paperclip, Donald Maclean, of MI6, one of the key people who helped set up NATO, defecting to Russia in 1951.[14]" Footnote 13 was "Gusenko, Igor, and Robert Bothwell. The Gouzenko Transcripts: the Evience Pres. to the Kellock-Tascherau Royal Commission of 1946. Deneau, 1982." Footnote 14 was "'LOST BRITON IS SAID TO ADMIT RED TIES; Lords Hear Missing Diplomat's Recording of the Statement Is in Hands of F. B. I.' 1952. The New York Times. The New York Times. October 29, 1952." Neither source said anything about Traub.

Next Finnegan wrote:

John Loftus says it was around this time, Traub began to get nervous, turning down top positions at the USDA's Plum Island, and this aroused the suspicion of military intelligence. Traub's release of large amounts of weaponized insects, such as ticks, mosquitoes, and mites, were carrying much more than harmless, benign tracers, and soon Traub's assistance in the States would be a cornered rat.

Author Linda Hunt was the first to bring forth the military's employment of Erich Traub and Operation Paperclip.[15] John Loftus exposed the Lyme disease connection to biological warfare in The Belarus Secret.[A] In 2004, author Michael Christopher Carroll likewise brought more attention to Erich Traub and the activities around Plum Island in Lab 257: The Disturbing Story of the Government's Secret Plum Island Germ Laboratory. Now, for the first time, in this book, John Loftus further tells the story of Traub's interrogation by Counter Intelligence Corps (CIC) Agent Dan Benjamin, to bring forth these startling new revelations of Erich Traub's confession to being a Soviet double-agent of the KGB:

Author Linda Hunt never got the credit she deserved for exposing Nazi scientists who had entered America under Operation Paperclip. Linda Hunt had been the first American journalist to visit Insel Reims, the secret island off the northern coast of Germany. This was where from 1945 onwards Nazi scientist Dr. Eric Traub and Stalin's biological warfare experts continued their joint research on immunological weapons.

Linda Hunt is the giant upon whose shoulders all future biowar researchers have stood. Several authors ripped off her research into the declassified intelligence files and then published her archival discoveries without citation under their own names. But I know the truth.

Ms. Hunt was first to warn the world about the dangers from the Paperclip scientists, but she was not the first one to warn me about the evil Dr. Traub. That credit belongs to Dan and Anne Benjamin, arguably the best husband-wife intelligence team before Bob Baer of CIA married a woman smarter than he was.

After WWII, Dan was an agent in the US Army's elite Counter Intelligence Corps (CIC), Dan became the senior CIC agent in charge of anti-communist intelligence for the American zone of occupied Germany, a position he later held for the entire European Command (EUCOM G-2) and then finally at the Pentagon where he was a Department of Army Civilian (DAC) who liaised with CIA.

The Pentagon thought that Dan's charming British wife, Anne, was "just a secretary." In fact, Anne did start as a secretary for the government in the British zone of occupied Germany. But, like her husband, her brilliance was soon recognized.

What Dan's friends in the Pentagon never knew was that Anne was recruited as an officer in the British Secret Intelligence Service (SIS or MI6). It was Anne who was in charge of the British secret intelligence archives for occupied Germany.

Anne received reports from Frederick "Freddy" Van Den Heuvel. Freddy was the SIS officer in charge of recruiting Nazi scientists, many of whom the British Government protected from prosecution as war criminals.

Freddy's best recruiting agent was Robert Maxwell who ran a German "publishing house" for scientific papers. Publication was a bait no scientist could refuse. Maxwell's publishing company for scientific papers was an SIS front to lure Nazis scientists to come out of hiding before the Russians could find them and drag them off to Moscow.[B]

By 1949, as the SIS archivist in post war Germany, Anne Benjamin had probably learned all that could be learned about SIS recruitment of Nazi scientists, including the evil Nazi genius, Dr. Traub. According to the SIS reports Anne received, the Russians had held Dr. Traub in custody in communist-controlled Eastern Europe after WWII, but SIS somehow arranged Traub's miraculous "escape" to West Germany.

Anne and her American husband, Dan Benjamin, were suspicious. By 1951, it was clear to them that that the senior SIS officers who approved Dr. Traub's escape from the Soviet Army's clutches were none other than Kim Philby and Donald Maclean, the highest-ranking communist spies inside British Intelligence.

Dan and Anne suspected (correctly) that it was this same "Cambridge Ring" of communist spies inside the SIS that had arranged Dr. Traub's immigration to America under Operation Paperclip. Kim Philby's underling (and lover) Donald Maclean was the SIS's scientific liaison to the Americans advising them which Nazis were worth recruiting.

[...]

No one in the Pentagon suspected at the time that Dr. Traub was perhaps the most villainous of all the Nazis to enter America. He was just a German veterinarian with some expertise in animal vaccines, a very profitable market for American pharmaceutical companies. The greed of Big Pharma to employ Nazi scientific experts like Traub led to the Benjamins' warnings being ignored. But soon the American military began to realize that Dan Benjamin may have been right to suspect that there was more to his story.

Dr. Traub had been recruited by Donald Maclean of the Cambridge Five Spy Ring inside SIS. Maclean, the communist agent, had advised the gullible Americans which German scientists should be brought to America under Operation Paperclip. When Maclean defected to Moscow in 1951, the Pentagon realized that Dan Benjamin was the only one who had been asking the right questions about the Nazi scientists whom McLean had sent to America, especially Dr. Traub. Dan Benjamin was asked by the Department of Defense to investigate why Dr. Traub had refused three times to accept a promotion for director of the biological laboratory on Plum Island between Connecticut and New York's Long Island. Was it because the Plum Island job required an intensive investigation for a Top-Secret clearance? Was there something in Dr. Traub's past that he feared would be discovered?

Dan Benjamin personally interrogated Dr. Traub. As the CIA will attest, Dan was probably the best interrogator in American intelligence. He never used torture or truth serums. Dan simply studied everything about his subject before he ever met him. Dan was friendly to Dr. Traub but made it clear to him that the actual interview was an unnecessary formality.

Dan already knew Traub's miraculous "escape" from communist East Germany had been arranged with the help of the communist spy ring inside British SIS. Dan briefly walked Traub through a few of the many contradictions and coverups in Traub's record. Did Dr. Traub have anything he wished to say for the record before he was handed over for sentencing as a spy for the KGB?

The bluff seemed to work. Dr. Traub decided to confess. He admitted that he had been captured by the Russian army at the end of WWII. He admitted that his fake escape from East Germany was arranged by Philby and Maclean because he promised to serve the Soviet Union as a communist spy inside American intelligence.

But Traub claimed he was such an unimportant little guy that the Russians never activated him for espionage. In fact, they never even bothered him again. Traub's explanation was that Soviet intelligence must have had so many other higher-level spies among the Nazi paperclip scientists, that the KGB never needed to contact a low-level veterinarian like him.

Traub said he repeatedly refused American promotions requiring any security clearance because he wanted to keep a low profile so the Russians would not bother with a little guy like him. It was a lie, but it was one that the Eisenhower administration desperately wanted to hear. Traub's public trial could have exposed the Dulles' brothers perfidious behavior.

Instead of following Dan's recommendation to prosecute Dr. Traub as a communist spy and investigate all the other German scientists, the Eisenhower administration ordered the Pentagon to accept Traub's rather dubious explanation. Nevertheless, the Army insisted that if Traub was not going to be sent to prison, at the very least Traub should be fired from all his American contracts and deported back to Germany where he should be placed under continuous surveillance and banned from any classified research.

Instead, The Eisenhower administration allowed Traub to continue serving as a UN health inspector. This UN status plausibly afforded Traub diplomatic immunity from American arrest as a confessed communist spy. To my shame, I did not give Dan's story about this seemingly minor Nazi scientist much priority for a follow up. Even though my time and funds were limited by my health, I did not give up entirely.

In the late 1980's I asked Rachel Verdon, one of my wonderful Lyme Disease volunteers, to request declassification of government records concerning Plum Island. Rachel discovered that nearly all the records were still classified or had been destroyed, including the bioweapons master file named "clandestine attacks on crops and animals" which had been illegally shredded.

Rachel also discovered many open-source documents confirming my sources insistence that the Russians had extensively studied tick-borne disease for more than a half century. Rachel's tireless research was not wasted as it did prove beyond any doubt that the US Government had built a brick wall of secrecy around whatever the communist double agents had done at Plum Island.

I did cooperate openly with another author in a wonderful book called Lab 257 but there was not much that I could tell him while the classification order was still in effect.

Even if Dan Benjamin had mentioned Traub's name, I had quite forgotten it for many years until I was accidentally reminded by Hollywood producers looking into Traub's background with tick experiments at Plum Island. How many German scientists under Operation Paperclip could there be who repeatedly declined promotions to be director of research at Plum Island? Traub had to be the same man who confessed to Dan that he was a spy for the KGB.

Dan and Anne had passed away before I could tell them that I had figured out why Traub never went to prison as a Nazi war criminal turned KGB spy. Traub was untouchable because he could blackmail the Eisenhower administration. It was Traub who designed the insect bombs that the US Air Force had dropped on North Korea and China. It was not his first such war crime.[16]

I hope I don't violate fair use by quoting such a large block of text, but there are multiple obervations I want to make about the text:

I didn't find information about Dan or Anne Benjamin by googling for combinations of terms like "Dan Benjamin" "Erich Traub" or "EUCOM G-2" "Dan Benjamin" or "Vanden Heuvel" "Anne Benjamin" or "Anne Benjamin" "John Loftus".

There is a real Dan Benjamin born in 1961, who was a "Coordinator for Counterterrorism" at the US Department of State, and who was earlier the German bureau chief for the Wall Street Journal and a German correspondent of TIME. [https://www.americanacademy.de/staff-member/daniel-benjamin/] He became a well-known author on terrorism after 9/11, and he is probably someone Loftus would have heard about, because both Loftus and Dan Benjamin are even mentioned in a Wikipedia article about allegations that Saddam Hussein was linked to Al-Qaeda. [https://en.wikipedia.org/wiki/Timeline_of_Saddam_Hussein_and_al-Qaeda_link_allegations] So I don't know if the Dan Benjamin born in 1961 served as an inspiration for Loftus's character of an American spy stationed in Germany.

Even in the case that the counterintelligence agent Dan Benjamin was a real person, his name sounds Jewish, and if he was in fact a Jew, then a Jewish counterintelligence agent is hardly a reliable source when it comes to information about Nazis. And even if Dan Benjamin was a real person, then his information is still unreliable because it was conveyed by Loftus, who has a habit of making up false information and saying he heard it from former spies.

Finnegan on Belarus Secret and Donald Maclean

Finnegan wrote in his book:

My source John Loftus was the first to expose the Lyme disease connection to biological warfare in 1982, in The Belarus Secret, and even noted it was being spread by ticks before it was publicly acknowledged, and the Plum Island experiments had been directed and overseen by one of our allies in British intelligence, a man named Donald Maclean, a confirmed double agent for Soviet Intelligence when he defected to Moscow in 1951:

A few months after it appeared in my book, scientists employed by the US Government published a report that confirmed that Lyme Disease was indeed being spread by ticks. However other government officials lied and denied any American tick experiments ever took place on Plum Island. It was a half-lie to conceal a sensitive political scandal.

The Plum Island experiments had been carried out by one of our allies in British intelligence, a man named Donald MacLean. He was confirmed as a double agent for Soviet Intelligence when he defected to Moscow in 1951.[...][66]

Footnote 66 was "John Loftus, Taken from the rough draft of Introduction to The Sleeper Agent [personal communication] 2022".

Willy Burgdorfer found Lyme disease to be transmitted by ticks in 1981 and published his findings in June 1982. [https://www.science.org/doi/abs/10.1126/science.7043737] I believe Loftus did not yet mention Lyme disease in the first edition of The Belarus Secret published in October 1982 but ony in the 1989 Paragon House edition.

But then why did Loftus himself say that the 1982 study was published a few months before the revelation that Lyme disease was spread by ticks appeared in his book? Is he somehow falsely trying to predate his revelations so he can take credit as the originator of the Lyme disease bioweapon theory?

Next Finnegan wrote:

Donald Maclean had been instrumental in the formation of joint-agreements between Britain, Canada, and the United States to share research and collaborate on nuclear, chemical, and biological development and testing, and all Top-Secret information relevant to it. Maclean was also appointed head of Chancery at the British Embassy in Cairo, Egypt,[67] a geographic location that would become significant as an intermediary area for biological warfare research taking place in Africa under the Navy's special unit, NAMRU-3.[68] John Loftus is here saying that Maclean was directing these tests, though not actually the one physically conducting the experiments, this was being done by other scientists after WWII, under his direction, and it was Erich Traub who supervised these tests when he came to America under Operation Paperclip which Loftus revealed in The Belarus Secret in 1982:

Even more disturbing are the records of the Nazi germ warfare scientists who came to America. They experimented with poison ticks dropped from planes to spread rare diseases. I received some information suggesting that the US tested some of these poison ticks on the Plum Island artillery range off the coast of Connecticut during the early 1950s. I explored the old spies' hypothesis that the poison ticks were the source of the Lyme disease spirochete, and that migrating waterfowl were the vectors that carried the ticks from Plum Island all up and down the Eastern Seaboard. Most of the germ warfare records have been shredded, but there is a top-secret US document confirming that "clandestine attacks on crops and animals" took place at this time. The Lyme disease outbreak in America was monitored secretly under the cover of a New England health study.[69]

Footnote 69 refers to America's Nazi Secret and not the original 1982 edition of The Belarus Secret. Finnegan gave the impression Loftus may have already mentioned in 1982 that Maclean oversaw the experiments, but I haven't found Loftus mentioning it anywhere before Finnegan's book.

In the sentence where Finnegan introduced the paragraph he quoted from America's Nazi Secret, he wrote that "John Loftus is here saying that Maclean was directing these tests", even though the paragraph didn't mention Maclean. And Loftus said the tests took place "during the early 1950s", but Maclean moved from the United States to Cairo in 1948, and I believe he never visited the United States again after 1948 (at least LLMs didn't find any evidence for it based on sources like his biographies).

In another part of his book, Finnegan wrote: "It is possible that all samples that were positive were from 1949-1951, only two samples specifically from 1946 were positive and we have covered the probability that Donald Maclean had Traub's weaponized ticks and spirochetes brought to America by 1945 when John Loftus indicates that British Intelligence was testing these ticks at Plum Island and surrounding areas." But in the paragraph in The Belarus Secret, Loftus said the tests took place in the early 1950s, and not 1945. If the tests would've taken place between 1944 and 1948 when Maclean lived in the United States, then did the Nazi scientists who took part in the tests not include Traub? Traub didn't move to the US until 1949. I'm fairly sure that Traub was never even in the United States at the same time as Maclean.

In other parts of the book when Finnegan wrote about Traub's connection to Maclean, Finnegan generally cited personal communication with Loftus, some other weak source, or no source at all:

I didn't even find evidence that Maclean was connected to biological research, or that he had any background in biology. Grok said:

Donald Maclean had no professional involvement whatsoever in biology, biological research, virology, microbiology, medicine, or any aspect of germ or biological warfare programs.

He was a career British diplomat and senior Foreign Office official whose entire professional life revolved around political, diplomatic, and nuclear policy matters. From 1944 to 1948, while serving at the British Embassy in Washington, D.C., Maclean held the sensitive position of joint secretary of the Anglo-American-Canadian Combined Policy Committee on Atomic Development. In that role he had access to highly classified information concerning the Manhattan Project, atomic energy policy, uranium supplies, and the early development of nuclear weapons. This nuclear intelligence formed by far the most valuable material he passed to Soviet intelligence. After leaving Washington in 1948, he was posted to Cairo as Head of Chancery, and upon his return to London in 1950 he became head of the American Department at the Foreign Office, dealing with NATO affairs and aspects of the Korean War. All of these responsibilities remained strictly within the spheres of diplomacy, international relations, and nuclear strategy.

Maclean's formal education consisted of a classical curriculum at Gresham's School in Norfolk followed by Trinity Hall, Cambridge, where he studied modern languages (French and German) and history. He received no university-level scientific training of any kind. Throughout his diplomatic career there is no record of him ever being assigned to, or even briefed on, any biological research programs, chemical weapons matters, or medical intelligence.

Claims suggesting that Maclean had any connection to biological weapons, Erich Traub, weaponized spirochetes, Plum Island, or related research appear exclusively in fringe conspiracy literature, particularly theories linking Lyme disease to U.S. government laboratories. These assertions are not supported by any declassified MI6, CIA, or FBI documents, nor by mainstream historical biographies such as Roland Philipps' A Spy Named Orphan or Robert Cecil's A Divided Life. Serious historians and intelligence scholars have found no evidence that Maclean ever dealt with biological topics in any capacity.

Erich Traub's research on tick-borne pathogens

When I showed Finnegan's timeline on Traub to Grok, and I asked what evidence the timeline contained that Traub was involved in research into Borrelia or tick-borne pathogens, Grok said: [https://www.thesleeperagent.com/erich-traub]

Finnegan (The Sleeper Agent timeline) presents the following claims as evidence linking Erich Traub to research on tick-borne pathogens or Borrelia. None of the entries describe Traub personally conducting extensive hands-on experiments weaponizing or modifying any tick-borne agents; most connections remain indirect, supervisory, or heavily interpretive.

1. 1939 - Learning about tick-borne diseases from Karl Beller

In 1939, while serving as assistant to Karl Beller at the University of Giessen, Traub allegedly received instruction on various tick-borne diseases. Finnegan claims Beller taught him about Rickettsia, Babesia, Bartonella, Ehrlichia, and the specific ticks capable of transmitting them. This knowledge is said to come from a chapter titled "Heartwater and Other Animal Rickettsioses" in the Handbook of Virus Diseases. The text further asserts that Beller demonstrated how multiple infections could be combined into a single complex syndrome and that hard-bodied ticks could transmit spirochetes. Finnegan interprets this exposure as foundational preparation for Traub's later supposed use of these agents in weaponized ticks released on the West.

2. 1939 - Access to avian spirochete (Borrelia anserina)

In 1939, Werner Schäfer, described as Traub's associate assistant and protégé at the University of Giessen, published a paper on maintaining avian spirochetes. The cited work is Schäfer 1939 - "The Maintenance of Spirochaeta gallinarum by Passages in Fowl Embryos." Schäfer reportedly received the strain from Dr. Franz Jahnel, and Finnegan states that Traub and Beller were Schäfer's superiors at the institute. The paper itself describes a practical method for keeping fully virulent strains alive in embryonated eggs instead of live chickens for teaching and research purposes. Finnegan interprets this as evidence that Traub came into possession of the avian spirochete (Spirochaeta gallinarum, later renamed Borrelia anserina), which he claims was later weaponized into Borrelia burgdorferi.

3. 1941 - Mention of blood parasites in the horse respiratory catarrh paper

In 1941, during an investigation of a respiratory outbreak in German Army horses belonging to a veterinary company, Traub and his colleagues reportedly conducted experiments that included checks for blood parasites along with equine infectious anemia and infectious respiratory catarrh. The paper is titled "Infectious Respiratory Catarrh in the Horses of a Veterinary Company" (Traub 1941). Finnegan highlights the inclusion of blood-parasite examinations as evidence of Traub's direct laboratory experience with such organisms. He links this work to possible familiarity with agents like Babesia, a common equine blood parasite, and suggests the study of mixed infections could have been useful for creating diagnostically confusing disease presentations.

4. 1953 USDA poultry conference listing avian spirochetosis as a biological warfare concern

In 1953, a USDA poultry conference on biological warfare threats listed avian spirochetosis (Borrelia anserina) among "special agents" of particular concern. Finnegan claims this listing proves that Traub's earlier work with the avian spirochete at Giessen was recognized as a potential bioweapon. He further asserts that this conference provides evidence that Lyme disease (Borrelia burgdorferi) originated from Traub's alleged weaponization of the avian strain, noting the complete absence of subsequent Plum Island research on Borrelia anserina despite the lab's mandate to study foreign animal diseases with zoonotic potential.

5. Vague references to Traub's 1950s U.S. Navy work on pathogens and rickettsia

During his employment at the Naval Medical Research Institute in the early 1950s, Traub was assigned as Supervisory Bacteriologist with responsibilities connected to maintaining approximately 40 strains of viruses and rickettsiae. Finnegan interprets this broad mandate as including tick-borne diseases, even though no specific tick-borne agents are named in the surviving job descriptions or publications from that period. He presents these duties as circumstantial support for the idea that Traub continued working with or supervising research on rickettsial and tick-related pathogens under U.S. Navy auspices.

6. Narrative ties in Traub's later papers on immune tolerance and mixed infections

In Traub's post-war publications on immune tolerance, lymphocytic choriomeningitis virus (LCM), Eastern equine encephalomyelitis (EEE), and related topics, Finnegan occasionally draws narrative connections to "stealth" or mixed/co-infections. These papers are interpreted as conceptually relevant to the creation of complex, diagnostically confusing diseases that could involve tick-borne pathogens. However, none of the actual papers describe direct research on ticks or Borrelia; the links remain purely interpretive and are used to bolster the overall story of Traub developing chronic, hard-to-detect infections.

Key Limitations Noted

All of the connections presented by Finnegan are indirect, relying on supervisory roles, incidental mentions, or broad institutional associations rather than primary evidence of Traub's own experimental work. No quotes or descriptions in the cited papers show Traub isolating, passaging, genetically altering, or weaponizing Borrelia, Babesia, or any other tick-borne pathogen. The 1941 horse paper, for example, mentions blood parasites only in passing while ruling out differentials during a respiratory outbreak and is not a dedicated study on Babesia or spirochetes.

So basically none of the six points showed that Traub himself was involved in research on tick-borne pathogens. Here's my own comments about the points:

  1. In his book Finnegan wrote: "Dr. Karl Beller published several additional chapters in the Handbook for Virus Diseases in 1939 while Traub was his assistant Professor. There was a chapter, 'Heartwater and other animal rickettsioses.' It is here that Erich Traub gained his important research on ticks and tick-borne disease." The book has an 18-page chapter titled "Herzwasser und sonstige tierische Rickettsiosen. Von Prof. Dr. K. BELLER - Gießen". [https://books.google.com/books?id=IBzZAAAAMAAJ&q=beller] But Finnegan didn't present evidence that Traub had even read the chapter about rickettsioses in the book, or that Beller did research on Rickettsia during the time he worked with Traub. When Finnegan wrote that Traub "gained his important research" from Beller, I think he meant that Traub might have gained knowledge to do research on tick-borne pathogens if he had read Beller's book chapter, because Finnegan didn't present evidence that Traub did any research on ticks during the time he worked with Beller. On his website Finnegan wrote: "1939 - Karl Beller teaches Traub all about the tickborne diseases like Rickettsia, Babesia, Bartonella, Ehrlichia, and the different ticks for spreading them. It was published in a chapter Heartwater and Other Animal Rickettsioses for the Handbook of Virus Diseases while Traub was his assistant. He teaches Traub how a complex disease results when many infections are rolled into one, citing a case where a dog was simultaneously infected with Rickettsia, Babesia, Bartonella, Ehrlichia, and Leishmaniasis, while also showing that it is possible to get hard-bodied ticks to spread spirochetes. All of these agents would later be used in Traub's weaponized ticks unleashed on the West." [https://www.thesleeperagent.com/erich-traub] But he didn't cite a source that Beller taught any of those things to Traub, so I don't know if Finnegan simply assumed that Traub would've learned about the subjects covered in the book chapter by reading the book chapter, or that if Beller was knowledgeable enough about rickettsioses to write a book chapter about them, then he would've likely also discussed them with Traub in person.

  2. Finnegan wrote that Traub was the supervisor of Werner Schäfer, who wrote a paper published in 1939 titled "Fortführung von Spirochaeta gallinarum-Stämmen von Eipassagen" ("The Maintenance of Spirochaeta gallinarum by Passage in Fowl Embryos"). The paper said: "Since we have to have a fully virulent Spirochaeta gallinarum strain in our institute for research and teaching purposes, we have tried to replace the expensive chicken passages with a complete, simple and cheap breeding procedure." But Finnegan didn't present evidence that Traub himself did any research on Spirochaeta gallinarum, which was later renamed to Borrelia anserina. On his timeline Finnegan wrote that Schäfer mentioned "that a fully virulent strain of Spirochaeta gallinarum was needed by his superiors at the University of Giessen for teaching and research purposes", even though in the part of the paper Finnegan quoted, Schäfer didn't seem to specify if the spirochetes were required by his superiors or by someone else, because Schäfer simply wrote that "we" at "our institute" needed to have a fully virulent strain of the spirochetes.

  3. In his book Finnegan wrote: "Traub mentions extensive experiments on horses with blood parasites in a 1941 paper, linking him to direct experience with disease agents like Babesia.[16] Adding a weaponized avian relapsing fever spirochete (Borrelia anserina) to the mix would cause a complex mix of infections that would not only be very confusing to physicians and diagnosis, but also very resistant to treatment." On his website he wrote: "An outbreak of unknown origin occurs in Army horses owned by a veterinary company, with horses showing signs of broncho-pneumonia. They set up a handful of experiments to assess the cause of disease. They set up experiments on blood parasites, equine infectious anemia, and infectious respiratory catarrh (mixed infections). They conclude the disease was due to infectious respiratory catarrh, after finding Streptococcus equi, Streptococcus pyogenes, and other bacterium that are usually considered 'harmless' to the horse." [https://www.thesleeperagent.com/erich-traub] The paper he cited was titled in German "Infectious Respiratory Catarrh in the Horses of a Veterinary Company". Infectious respiratory catarrh in horses is typically caused by viruses or bacteria. But because the study also investigated blood parasites as an alternative etiology, and Babesia are tick-borne blood parasites, Finnegan said that the study linked Traub "to direct experience with disease agents like Babesia" (but he didn't even specify if the study investigated Babesia as a possible cause or only "agents like Babesia").

  4. Finnegan wrote that the JIOA file on Traub's assistant Anne-Lise Bürger said: "Duties of the position to be filled by Miss Burger are concerned with the supervision of maintenance of approximately 40 strains of virus and rickettsias [sic] in serial egg and animal passages in order to provide stocks of infectious materials for experimental work in [the] virology division and other divisions of the Naval Medical Research Institute." However it's not clear if Bürger would've even maintained strains of Rickettsia for Traub or for other researchers. The file specifically mentioned that the stocks were needed by other divisions at the institute and not only the virology division, but Traub appears to have primarily worked on virological research at the institute, even though I don't know if his work was conducted exclusively under the auspices of the virology division or not. And in any case, it's not even clear if Bürger ever moved to the United States. Linda Hunt wrote that Traub and Bürger's "work for the Navy included conducting experiments on animals to determine the lethal doses of more than forty strains of highly infectious viruses", where she cited the JIOA file on Bürger, but the file was dated 1950 before Traub is supposed to have even moved to the United States, so at best the file would've described the work Traub was going to do with Bürger in the future. [https://lust-for-life.org/Lust-For-Life/_Textual/LindaHunt_SecretAgenda-TheUnitedStatesGovernmentNaziScientistsAndProjectPaperclip1945To1990_1991_178pp/LindaHunt_SecretAgenda-TheUnitedStatesGovernmentNaziScientistsAndProjectPaperclip1945To1990_1991_178pp.pdf] The part of the file Finnegan quoted didn't even speak of "more than forty strains of highly infectious viruses" but "approximately 40 strains of virus and rickettsias", and the text quoted by Finnegan didn't speak of determining lethal doses of the pathogens but only maintaining stocks of pathogens. I didn't find the full JIOA file published anywhere online.

  5. In his book Finnegan wrote that in a USDA conference in 1953, Colonel Frank A. Todd said: "I believe that records indicate that several foreign poultry diseases have gained entrance into this country by the importation of undeclared laboratory cultures, from smuggled birds, and from importing insect vectors and birds during the carrier stage or during the incubation period. We also know that raw garbage, contaminated feeds and veterinary biologics have been factors in spreading disease in this country." Finnegan didn't mention Todd saying anything about Borrelia, but Finnegan wrote: "The pathogens that the USDA officials were most concerned about in 1953, included fowl plague virus, Newcastle Disease Virus (NDV), avian spirochetosis (Borrelia anserina), avian malaria (Plasmodium gallinaceum, Plasmodium lophurae), Eastern Equine Encephalitis Virus (EEE), ornithosis (chlamydia pneumoniae, psittacosis), and botulism.[20] Spirochetosis appeared to be a major concern in poultry,[21] for perhaps the only time they admit it on record from that point forward, and a main part of the attack had a lot to do with Traub's weaponized spirochetes." Footnote 20 referred to a document about foreign avian diseases published by the USDA, which included a brief description on methods for diagnosing different types of diseases in birds, which included a single sentence about avian spirochetosis. But the document didn't mention that avian spirochetosis was a major concern, and it didn't specifically even name Borrelia anserina or Spirochaeta gallinarum. [https://archive.org/details/CAT10678555/page/n32] Footnote 21 referred to a paper about an outbreak of avian spirochetosis in turkeys in California. The paper was published in a journal of the American Veterinary Medical Association, and not by the USDA, even though Finnegan suggested that the USDA had somehow admitted in the paper that spirochetosis was a major problem in birds. [https://www.cabidigitallibrary.org/doi/full/10.5555/19542200711] The American Veterinary Medical Association is not even a governmental organization.

  6. The rest of the timeline didn't directly describe Traub working with tick-borne pathogens either. Finnegan mentioned that in 1972 Traub gave a lecture about the history of LCM where he mentioned that ticks were able to transmit LCM. [https://link.springer.com/chapter/10.1007/978-3-642-65681-1_1] About a fourth of the lecture was visible as a free preview, but it didn't include any reference to ticks, so Traub may have only mentioned ticks in passing, and he likely did not discuss personally researching tick-borne transmission of LCM.

One piece of evidence that was missing from Grok's list of six points was a paragraph Finnegan quoted from Lab 257, where Mike Carroll claimed that an anonymous eyewitness said that a Nazi scientist had released ticks on Plum Island. But Carroll didn't even make it clear if the eyewitness was talking about Traub or some other Nazi scientist, and eyewitness testimony of nefarious actions by Nazis has often turned out to be fabricated. And a major problem with the story is that Finnegan claimed that Donald Maclean oversaw the tests where the ticks were released, but Maclean had already moved out of the United States by the time Traub moved into the United States.

Traub's assistant Anne-Lise Bürger

Finnegan wrote in his book:

Additional references to his work on tickborne diseases can be found in the Navy's approval to hire his former Insel Riems technical assistant, Anne-Lise Bürger. Bürger was approved for work on American shores under contract with the Naval Research Institute to assist Traub in matters of biological warfare, with an impressive resumé in biological research, including rickettsia, a tickborne disease:

Duties of the position to be filled by Miss Burger are concerned with the supervision of maintenance of approximately 40 strains of virus and rickettsias [sic] in serial egg and animal passages in order to provide stocks of infectious materials for experimental work in [the] virology division and other divisions of the Naval Medical Research Institute.[44]

There are, as of yet, no records showing that Bürger ever actually made it to the United States, because much of Traub's published research for the Navy lists Worth I. Capps as his technical assistant.[45] Bürger is never mentioned, nor thanked in any of his American publications, as well as the fact that Bürger published a research paper with Bernard Schneider in 1951[46] when she had been approved in November/December of 1950. She published a follow-up paper with Schneider the same year, with her name changed to Anne-Lise Schneider, indicating she married Bernhard Schneider and stayed at Behringwerke AG.[47] It is a good probability more will be discovered at a later time, but probably not until after this book has been published.

What is significant in Bürger's file, however, is that it is here we find a direct reference to the tick-borne disease class of bacteria, rickettsia, tying a direct link to Erich Traub's Navy work, because essentially, she was to be conducting these tests for Erich Traub, working as his technical assistant. Moreover, this same document establishes, for the record, that there were no scientists skilled enough in America to replace the work she and Traub were doing, and this will become significant when we discuss Willy Burgdorfer's role. It states:

In view of past long association in the fields of bacteriology and virology with Dr. Erich Traub, whom she will assist at the Institute, Miss Bürger's assignment here cannot be as adequately filled by any personnel available in the United States.[48]

Footnotes 44 and 48 both refer to the same document: "National Archives, Joint Intelligence Objectives Agency, J.I.O.A. Administrative Records. (1950). Memorandum on Anne Bürger, C. F. Berrens, Naval Medical Research Institute, to Chief of Naval Operations, 27 November 1950, Navy Escape Clause (RG 330). NARS."

In Lab 257, Mike Carroll wrote: "With his 'laboratory assistant' Anne Burger, who came over in 1951, Traub experimented with over forty lethal viruses on large test animals.[4]" Footnote 4 says: "Linda Hunt, author of Secret Agenda, the seminal book on Project PAPERCLIP, believes Burger may not have been Traub's 'assistant,' but rather his mistress. Apparently other PAPERCLIP recruits had imported their mistresses from Germany along with their families when they came to America. No additional information is available to the public on Anne Burger."

In the book Secret Agenda, Linda Hunt wrote: "In addition to the Air Force group, the Navy brought several biological warfare experts to the United States in the 1950s under Paperclip. For example, Anne Burger arrived in 1951 to work for a Navy biological warfare project at the Naval Medical Research Institute in Bethesda, Maryland. Burger had been a wartime assistant to Paperclip scientist Erich Traub, who arrived earlier. Their work for the Navy included conducting experiments on animals to determine the lethal doses of more than forty strains of highly infectious viruses.[35]" [https://lust-for-life.org/Lust-For-Life/_Textual/LindaHunt_SecretAgenda-TheUnitedStatesGovernmentNaziScientistsAndProjectPaperclip1945To1990_1991_178pp/LindaHunt_SecretAgenda-TheUnitedStatesGovernmentNaziScientistsAndProjectPaperclip1945To1990_1991_178pp.pdf] Footnote 35 is: "Anne Burger biography and biological warfare job description: memo, C. F. Berrens, Naval Medical Research Institute, to Chief of Naval Notes 305 Operations, 27 November 1950, JIOA administrative files, Navy Escape Clause, RG 330, NARS. Erich Traub biography is in Traub's JIOA dossier, RG 330, NARS."

I didn't find the JIOA file published anywhere. The JIOA file was dated November 1950 but Hunt said Bürger arrived to the United States in 1951, so maybe Hunt relied on some other source as evidence of when Bürger arrived to the United States, or maybe the JIOA file said that Bürger was going to arrive to the US in 1951 so Hunt assumed that Bürger ended up moving to the US in 1951.

Finnegan's footnote 46 was "Schneider, Bernard, and Anne L. Bürger. 'Uber Das Serologische Verhalten Des Maul- Und Klauenseuche-Huhnereivirus Und Seine Verwendung in Form Der Adsorbat-vakzine Zur Immunisierung Von Rindern [Serological Behavior of Foot-and-mouth Disease Hen-egg Virus and Its Use in the Form of Absorbate Vaccine to Immunize Cattle].' Mh Prakt. Tier 3, no. 35 (1951): 35-40. Accessed August 3, 2019". Footnote 47 was "Schneider, B. & A. L. Schneider. Züchtung des Virus der Maul- und Klauenseuche vom Typ A (Vallée) im bebrüteten Hühnerei. Mhefte prakt. Tierhk. 3, 206. (1951)". I didn't find either paper posted online. The title of the second paper is similar to a paper by E. Traub and B. Schneider published in 1948 titled "Züchtung des Virus der Maul- und Klauenseuche im bebrüteten Hühnerei" (which is only missing the text "vom Typ A (Vallée)" that refers to serotype A in Vallée's classification scheme of FMD). [https://www.semanticscholar.org/paper/Z%C3%BCchtung-des-Virus-der-Maul-und-Klauenseuche-im-Traub-Schneider/c6ae0cc5cd076a6acb761756837baca76a7dfa17] So in the scenario where Bürger moved to the United States in 1951, she might have still been credited in the paper published in 1951 if the work in the paper had been done before 1951.

People listed in Finnegan's acknowledgements

In the acknowledgements section of The Sleeper Agent, Finnegan wrote: "I thank my source and book project friends, John Loftus, Crystal Bennett, Jody Savin, thank you for all the support and help with research materials and advice and suggestions." [https://books.google.com/books?id=aTKdEQAAQBAJ&pg=PT421] He also listed some of his personal friends and family, some emo bands, Kris Millegan, and these conspiracy people: "I thank Professor Richard B. Spence, Richard Grove and Autonomy, Mark Passio and the One Great Work Network, Marja West, Angie and Jim from Victurus Libertas channel, actor and friend Steve Shellen, thanks to Randy Williams at Old Colony."

I don't know why Finnegan listed Rick Spence first. Spence's bio says: "Professor Spence has been a commentator and consultant for the HISTORY® network, the International Spy Museum, and Radio Free Europe/Radio Liberty." [https://www.library.pima.gov/wp-content/uploads/sites/6/2020/09/Real-History-of-Secret-Societies-8680.pdf] The combination of History Channel, International Spy Museum, and Radio Liberty is reminiscent of the milieu John Loftus was moving in. Two of the main villains of The Belarus Secret worked for Radio Liberty, so they may have been in on the scheme and agreed to play the role of villains without busting the hoax by Loftus (and even though one of them had already died before Loftus published his book, he had still earlier played the role of a villain in the anti-Nazi propaganda campaign that Loftus built on in his book). Spence's work with the History Channel makes him into another Trine Day author who has appeared on mainstream media, like John Loftus and Peter Levenda. The website of the Intelligence Summit now gets redirected to the blog of Brent Beleskey, who worked as the producer of the Intelligence Summit and SpyCruise events, but SpyCruise was organized by the Centre for Counterintelligence and Security Studies, whose founder David Major is on the board of the International Spy Museum.

Rick Spence was a fellow of the anti-terrorism program of the Foundation for the Defense of Democracy in Tel Aviv, and he received a Naval Reserve Officers' Training Corps Faculty Excellence Award. [https://www.theothersideofmidnight.com/tosn-138/]

Finnegan posted two reviews of books by Spence on OGWN. [https://onegreatworknetwork.com/adam-finnegan/book-review-wall-street-and-the-russian-revolution-1905-1925-by-richard-b-spence, https://onegreatworknetwork.com/adam-finnegan/book-review-aleister-crowley-british-intelligence-and-the-occult-by-richard-b-spence] Spence also wrote the afterword to a book called Houses of the Holy whose author is a "former Air Force Special Operations pilot", but the website of the book prominently features both a video about the book by Finnegan and a text review of the book by Finnegan. [https://housesoftheholy.net]


Added later: Finnegan posted this response to me: [https://x.com/AWFinnegan/status/2037653546921812053]

But I'm not yet sure if he is deliberately producing disinformation, or he is just a useful idiot who is being fed disinformation by Loftus. Therefore I have been looking into his connections to people in the conspiracy movement to see if he is linked to people who are likely to be controlled opposition. For example his connection to Rick Spence is highly suspicious. It's also suspicious how he said he was going to be working with mystery schools, and how he wrote for the website of Mark Passio, who is the son of a special operations officer and who was a priest in Anton LaVey's church.

Did Himmler send Traub on a trip to Turkey?

In his book Finnegan wrote: "In Dr. Kurt Blöme's talks with Heinrich Himmler, commander of the SS-Waffen (Schutzstaffel) regarding biological warfare, it was decided to secure strains of rinderpest, but securing it was not so easy. The obstacle was due to established laws across Europe forbidding them from storing the virus due to its highly contagious nature that could wipe out Europe's livestock, which gave them great difficulty in finding strains, and eventually, Himmler decided to send Traub on a trip to Turkey to secure cultures of rinderpest and he made the long journey there and back.[72] Nearing the end of the war, Himmler, had been pushing for more aggressive biological warfare development with his medical and agricultural authorities, Kurt Blöme, Walter Schrieber, and Otto Waldman." Footnote 72 was: "National Archives. Joint intelligence Objectives Agency (JIOA), JIOA Administrative Records. (n.d.). Interview of ALSOS Scientists: Dr. Kurt Blöme (RG 330 INSCOM dossier XE001248). NARS."

When I asked Grok what other documents support the claim that Traub took a trip to Turkey, Grok answered:

The account of Erich Traub's trip to Turkey to secure rinderpest virus strains for Nazi biological warfare efforts originates almost exclusively from a single postwar interrogation of Dr. Kurt Blome by ALSOS mission scientists. This interview is preserved in the Joint Intelligence Objectives Agency administrative records at the National Archives, specifically under RG 330 INSCOM dossier XE001248. Blome described how strict European laws prohibiting storage of the highly contagious rinderpest virus - due to its potential to devastate livestock - made acquisition difficult. When efforts stalled, Himmler ordered Traub to travel to Turkey, where he reportedly obtained cultures before returning to Germany. No contemporaneous German documents, such as travel authorizations, Riems Island laboratory logs, shipping manifests, or reports from other participants, have been identified in declassified archives to independently confirm the mission.

Secondary historical literature consistently traces the episode back to this same Blome statement without adding fresh primary evidence. Michael Christopher Carroll's 2004 book Lab 257 dramatizes Traub's search along the Black Sea coast of Turkey for a virulent strain intended for use against the Allies. However, it relies directly on the ALSOS-derived intelligence and introduces no new archival citations or independent verification. Such accounts often note that the acquired strain proved nonvirulent upon testing at Riems, leading to the abandonment of rinderpest weaponization in favor of continued work on foot-and-mouth disease. Amanda Kay McVety's 2018 scholarly study The Rinderpest Campaigns incorporates the Turkey trip into the broader context of wartime biological research. It acknowledges Blome's limited recollection of acquisition details while accepting the mission under Himmler's push for aggressive development involving Walter Schreiber and Otto Waldmann. McVety's analysis draws from the same postwar intelligence files rather than distinct sources such as Turkish veterinary records, border documentation, or Allied intelligence summaries that could corroborate Traub's movements independently.

Additional works on Operation Paperclip and Nazi scientist dossiers, including Linda Hunt's Secret Agenda and various accounts referencing RG 330 materials, mention the episode only within the framework of Blome's interrogation and Traub's role as lab chief at Riems. These texts provide interpretive context on the biological warfare program but do not present supplementary paperwork such as visa records, expense reports, or Soviet-zone postwar intelligence to verify the journey on its own. Wikipedia entries and derivative summaries uniformly echo the same limited sourcing, often citing Carroll's Lab 257 or the underlying National Archives file.

The earliest reference I found to the RG 330 dossiers of both Kurt Blome and Erich Traub was in Tom Bower's 1987 book The Paperclip Conspiracy: The Hunt for the Nazi Scientists, even though Linda Hunt had earlier referred to Blome's interrogation by ALSOS without mentioning the RG 330 identifier.

Tom Bower is a Jew who worked for 25 years for BBC Television. [https://en.wikipedia.org/wiki/Tom_Bower] Two of his books about post-war Nazis were serialized in The Times, and one of the books was made into a BBC TV documentary. So he has a similar background of working in mainstream media as Linda Hunt, Mark Aarons, John Loftus, and Paul Manning. He said that he was "once known as 'Tommy the Red', the Marxist involved in the student occupation of the London School of Economics 50 years ago". [https://www.newstatesman.com/politics/2019/02/tom-bower-s-diary-my-marxist-past-abuse-tariq-ali-warning-meghan-and-demise] He is married to a baroness who was the editor of the Evening Standard newspaper, and who was the senior advisor to Boris Johnson in 2012-2016. [https://en.wikipedia.org/wiki/Veronica_Wadley%2c_Baroness_Fleet]

Some of the intelligence documents that were supposedly discovered in the 80s might have actually been fabricated in the 80s. It's suspicious how the documents played a central role in the dramatic narratives presented by Linda Hunt and Tom Bower, who both worked in TV. The story of Traub's trip to Turkey is also told in Linda Hunt's book.

The National Archives has published a listing of 1,704 files in the RG 330 group which includes files for Blome and Traub, but I didn't find either file published online. [https://www.archives.gov/files/iwg/declassified-records/rg-330-defense-secretary/foreign-scientist-case-files.pdf]

Linda Hunt's 1985 article about Project Paperclip didn't mention the RG 330 identifier, even though the sources she cited included a "Secret Alsos Report B-C/250, 'Interrogation of Blome;' July 30, 1945.". [https://epizodyspace.ru/bibl/inostr-yazyki/bulletin-of-the-atomic/1985/hunt_us_coverup_of_nazi_scientists-no_04.pdf] When I googled for "Alsos" "B-C/250", the only other reference to the document I found was in a paper by Erhard Geissler, which included this citation: "'Subject: Interrogation of Blome, Director of German B.W. Activities. Information on Prof. Hornung,' Report No. B-C/250, 30 July 1945, Alsos Mission, p. 16." [https://www.cambridge.org/core/journals/politics-and-the-life-sciences/article/german-flooding-of-the-pontine-marshes-in-world-war-ii-biological-warfare-or-total-war-tactic/C783556F800988B9D617B8E10A0A5843]

Finnegan gave this citation for Blome's RG 330 file: "National Archives. Joint intelligence Objectives Agency (JIA), JIOA Administrative Records. (n.d.). Interview of ALSOS Scientists: Dr. Kurt Blöme (RG 330 INSCOM dossier XE001248). NARS." I didn't find the XE001248 identifier mentioned before 1990 at Google Books. [https://www.google.com/search?q=%22XE001248%22+before%3A1995&udm=36] Grok said "These 'XE' prefixes and sequential dossier numbers were used by Army Counterintelligence Corps (CIC) and later INSCOM elements primarily in the late 1940s through the 1960s for tracking sensitive personnel and security files." The identifier XE001248 was also mentioned on a list of files in the Investigative Records Repository, which was a US Army facility that stored counterintelligence files. [https://www.archives.gov/iwg/declassified-records/IRR%20Personal%20Name%20List_1.html]

The National Archives adopted the RG numbering system in the 40s. [https://prologue.blogs.archives.gov/2024/10/23/the-origins-of-the-record-group/] So both the RG and XE identifiers should've existed long before the 80s, even though of course it's not surprising that there would be no earlier references to the XE identifier or to Blome's RG 330 dossier, if the files in the dossier were classified before the 80s.

In 2013 when someone tried to do two FOIA requests to the CIA for files about Blome including the RG 330 file, both times the CIA replied: "The request has been rejected, with the agency stating that it can neither confirm nor deny the existence of the requested documents." [https://www.muckrock.com/foi/united-states-of-america-10/foia-request-regarding-kurt-blome-files-8638/] If Finnegan has access to the RG 330 documents, he should upload them somewhere online like at archive.org. Under US law, documents created by the federal government are not eligible for copyright and they are automatically in the public domain.

Did Borrelia anserina become Borrelia burgdorferi?

Response by Grok

In chapter 6 of his book, Finnegan wrote: [https://books.google.com/books?id=aTKdEQAAQBAJ&pg=PT139]

As an assistant professor under Beller at Giessen, Traub had a few students under him, such as Dr. Werner Schäfer, who went to Africa in 1939, and returned by the start of the war to later join Traub at Insel Riems.[5] He and Traub would also publish a paper that year on the virus of LCM in mouse blood.[6]

It was at this time Schäfer retrieved a strain of avian spirochetes, Borrelia anserina, then known as Spirochaeta gallinarum, which was given to him by Rockefeller-funded psychologist, Franz Jahnel. This was the spirochete from birds that was weaponized by Traub and would become in later years, Borrelia burgdorferi, the agent responsible for Lyme Disease, later supported by evidence in a 1989 publication, "Shared flagellar epitopes of Borrelia burgdorferi and Borrelia anserina."[7] Schäfer began growing the spirochetes in chick embryos, acknowledging their need, for a cheap way to maintain the spirochete and to have a fully virulent strain for research and teaching purposes. The results were published in "The Maintenance of Spirochaeta gallinarum by Passages in Fowl Embryos:"

Since we have to have a fully virulent Spirochaeta gallinarum strain in our institute for research and teaching purposes, we have tried to replace the expensive chicken passages with a complete, simple and cheap breeding procedure.[8]

When I pasted the text to Grok and asked if it is possible for Borrelia anserina to become Borrelia burgdorferi, Grok replied:

No, it is not possible for Borrelia anserina to "become" Borrelia burgdorferi. These are two distinct bacterial species within the genus Borrelia, and the claim that one transformed or evolved directly into the other - particularly through work by Erich Traub or Werner Schäfer involving weaponization or lab manipulation - is not supported by scientific evidence.

Borrelia anserina (formerly known as Spirochaeta gallinarum) causes avian spirochetosis, a disease primarily affecting birds (e.g., poultry like chickens and geese). It is transmitted by argasid (soft) ticks and has been known since the late 19th century.

Borrelia burgdorferi (more precisely Borrelia burgdorferi sensu stricto, with related species in the B. burgdorferi sensu lato complex) causes Lyme disease in humans and other mammals. It is transmitted by hard ticks (primarily Ixodes species) and was first identified as a distinct pathogen in the early 1980s by Willy Burgdorfer.

The 1989 paper titled "Shared flagellar epitopes of Borrelia burgdorferi and Borrelia anserina" (published in Veterinary Microbiology) demonstrates antigenic cross-reactivity - specifically, the two species share at least two epitopes on their flagella. One of these shared epitopes is not found in other Borrelia species like B. hermsii or B. coriaceae. This is based on studies using mouse immune sera and monoclonal antibodies in immunoblots.

This shared antigenicity reflects evolutionary relatedness within the Borrelia genus (both are spirochetes), but it does not mean one species can convert into the other, nor does it indicate genetic transformation, mutation under lab conditions, or weaponization leading to Lyme disease. Flagellar proteins (like the 41-kDa flagellin) are conserved across many spirochetes, leading to cross-reactions in diagnostics, but the bacteria remain separate species with different hosts, vectors, diseases, and genomic profiles.

The quoted passage about Schäfer maintaining Spirochaeta gallinarum (i.e., B. anserina) in chick embryos for research and teaching purposes aligns with historical veterinary microbiology practices - chick embryos were a common, inexpensive method to propagate certain pathogens before modern cell culture techniques. There is no credible evidence linking this to creating or modifying a Lyme disease agent.

Grok said that the time to the most recent common ancestor of anserina and burgdorferi is estimated to be millions of years ago, so it wouldn't have been possible to create burgdorferi from anserina through serial passage within a time span of a few years, and the diversity between different strains of Borrelia burgdorferi is so great that the strains cannot have had a common ancestor less than a hundred years ago:

The genetic distance between Borrelia burgdorferi (the primary agent of Lyme disease) and Borrelia anserina (the agent of avian spirochetosis) is substantial, reflecting their placement in separate major clades within the Borrelia genus: Lyme disease-associated (B. burgdorferi sensu lato, or LB group) versus relapsing fever-associated (RF group, where B. anserina resides as a classic avian/soft-tick transmitted species).

16S distance

The 16S ribosomal gene is commonly employed for taxonomical analysis of bacteria. When I searched GenBank for (borrelia[organism] OR borreliella[organism]) 16s 1300:1600[slen], there were a total of 2,166 results. [https://www.ncbi.nlm.nih.gov/nuccore/?term=%28borrelia%5Borganism%5D+OR+borreliella%5Borganism%5D%29+16s+1300:1600%5Bslen%5D] I downloaded the results by clicking "Send to:", clicking "File", and switching "Format" to "FASTA".

I then excluded plasmids, shotgun sequences, and intergenic sequences, aligned the remaining sequences, and I made a percentage identity matrix of the sequences. I thinned out the matrix to remove sequences that had over 99.7% identity to any previous sequence in the matrix, which retained 126 sequences. Then when I sorted the results based on their percentage identity to a common reference isolate of B. burgdorferi, it had about 99% identity to other species of Borrelia in the LB group, like afzelii, americana, andersonii, bavariensis, californiensis, garinii, lanei, lusitaniae, maritima, mayonii, spielmanii, tanukii, turdi, and yangtzensis. But the reference isolate of B. Burgdorferi had only about 96-97% identity to B. anserina:

# exclude plasmids, shotgun sequences, and intergenic spacers, remove duplicates, ensure
# reference isolate B31 is included and not one of its duplicates, and align result
brew install seqkit mafft
seqkit grep -nrivpshotgun,plasmid,spacer sequence.fasta|seqkit replace -ispn -r-|
cat <(seqkit grep -nrpB31 sequence.fasta) -|
seqkit rmdup -s|mafft --thread 7 --quiet ->borre.fa

# compile a utility for making a TSV percentage identity matrix of aligned sequences
curl -Ls sars2.net/f/pid.cpp>pid.cpp;g++ pid.cpp -O3 -o pid

# thin out a TSV percentage identity matrix to remove sequences with higher than
# specified identity percent to any previous sequence
thin()(awk -F\\t 'NR>1{for(i=2;i<NR;i++)if($i>x)next;print$1}' x="${1-99}" "${@:2}")

# omit sequences with over 99.7% identity to any previous sequence, and sort by distance
# to the B31 reference isolate of _Borrelia burgdorferi_
./pid<borre.fa>borre.pid
thin 99.7 <borre.pid|cut -d' ' -f1|seqkit grep -f- borre.fa|./pid|
awk -F\\t 'NR==1{for(i=2;i<=NF;i++)if($i~/B31/)break;next}{print$i,$1}'|sort -rn|
sed 's/, \(complete\|partial\) sequence.*//'
100.0000 AF467957.1 Borrelia sp. B31 16S ribosomal RNA gene
99.6873 M89938.1 Borrelia burgdorferi (VS219) rRNA sequence
99.6134 AF467971.1 Borrelia sp. MOD-1 16S ribosomal RNA gene
99.5595 NR_116166.1 Borreliella americana strain SCW-41 16S ribosomal RNA
99.5490 AF467970.1 Borrelia sp. SCGT-10 16S ribosomal RNA gene
99.5228 NR_158115.1 Borreliella lanei strain CA28-91 16S ribosomal RNA
99.5228 NR_148824.1 Borreliella californiensis strain CA446 16S ribosomal RNA
99.5188 KY348800.1 Borreliella garinii isolate Vanino_2011-11 16S ribosomal RNA gene
99.4709 NR_152696.1 Borreliella mayonii strain MN14-1420 16S ribosomal RNA
99.4547 AJ224136.1 Borrelia burgdorferi sensu lato, 16S rRNA gene, isolate CA2
99.4502 M60969.1 B.burgdorferi 16S ribosomal RNA
99.4148 D67018.1 Borrelia garinii DNA for 16S ribosomal RNA
99.3852 KY622012.1 Uncultured Borrelia sp. clone YN67 16S ribosomal RNA gene
99.3473 NR_170496.1 Borrelia maritima strain CA690 16S ribosomal RNA
99.3443 OL721871.1 Candidatus Borrelia sibirica isolate Alt17-64 16S ribosomal RNA gene
99.3434 NR_036806.1 Borreliella lusitaniae strain Poti B2 16S ribosomal RNA
99.2912 AF467969.1 Borrelia sp. SCGT-8a 16S ribosomal RNA gene
99.2857 AB178151.1 Borrelia garinii gene for 16S rRNA
99.2821 AJ009753.1 Borrelia garinii (isolate Far04) 16S rRNA gene, partial
99.2658 HM802226.1 Borrelia americana strain SCW-30h 16S ribosomal RNA gene
99.2268 AF467975.1 Borrelia sp. MOS-1b 16S ribosomal RNA gene
99.1947 D67024.1 Borrelia turdi DNA for 16S ribosomal RNA
99.1863 OR226552.1 Uncultured Borreliella sp. clone N11 16S ribosomal RNA gene
99.1222 D67023.1 Borrelia tanukii DNA for 16S ribosomal RNA
99.1222 D67021.1 Borrelia sp. DNA for 16S ribosomal RNA
99.0985 X57404.1 Borrelia burgdorferi 16S rRNA, partial
99.0660 AB037126.1 Borrelia sp. TM1 gene for 16S rRNA
99.0560 L40596.1 Borrelia burgdorferi 16S ribosomal RNA (16S rRNA) gene
99.0483 AB030751.1 Borrelia tanukii gene for 16S rRNA
99.0399 LC572078.1 Borrelia yangtzensis OP-014 gene for 16S rRNA
99.0181 MW301929.1 Borreliella garinii isolate 382 16S ribosomal RNA gene
98.9865 EU135597.1 Borrelia yangtzensis strain QTMP2 16S ribosomal RNA gene
98.9751 D67019.1 Borrelia afzelii DNA for 16S ribosomal RNA
98.9731 AB111523.1 Borrelia garinii gene for 16S rRNA
98.9612 NR_044732.2 Borreliella burgdorferi strain ATCC 35210 16S ribosomal RNA
98.9494 NR_104871.1 Borreliella spielmanii strain PC-Eq17N5 16S ribosomal RNA
98.9432 AB037125.1 Borrelia sp. TA1 gene for 16S rRNA
98.9019 MZ146350.1 Borreliella garinii isolate TC-T-119 16S ribosomal RNA gene
98.8862 EU085417.1 Borrelia carolinensis isolate SCCH-10 16S ribosomal RNA (rrs) gene
98.8771 AB037123.1 Borrelia sp. KR1 gene for 16S rRNA
98.8620 NR_118688.1 Borreliella japonica strain HO14 16S ribosomal RNA
98.8304 NR_118689.1 Borreliella andersonii strain 21038 16S ribosomal RNA
98.8183 LC572071.1 Borrelia yangtzensis IG-213 gene for 16S rRNA
98.7524 MH781146.1 Borreliella burgdorferi isolate CA8 16S ribosomal RNA gene
98.7170 L46695.1 Borrelia japonica (isolate IKA2) 16S ribosomal rRNA
98.7162 EU135593.1 Borrelia yangtzensis strain QLZSP1 16S ribosomal RNA gene
98.7032 PQ849842.1 Uncultured Borrelia sp. clone JX88 16S ribosomal RNA gene
98.6582 AB178152.1 Borrelia afzelii gene for 16S rRNA
98.6142 M72396.1 Borrelia sp. 16S small subunit ribosomal RNA
98.5666 MZ146347.1 Borreliella valaisiana isolate TC-T-02 16S ribosomal RNA gene
98.5412 AJ225165.1 Borrelia sp. 16S rRNA gene
98.3168 KY563168.1 Borreliella burgdorferi isolate 11-1019 16S ribosomal RNA gene
98.3142 L40597.1 Borrelia japonica 16S ribosomal RNA (16S rRNA) gene
98.1989 AM182231.1 Borrelia spielmanii partial 16S rRNA gene, strain PJes
97.9111 U28501.1 Borrelia burgdorferi strain ESP-1 16S ribosomal RNA gene
97.6036 L40598.1 Borrelia japonica 16S ribosomal RNA (16S rRNA) gene, partial rRNA
97.2465 AB473531.1 Borrelia sp. Tick98M gene for 16S rRNA
97.1935 LC905312.1 Borrelia sp. C15 gene for 16S ribosomal RNA
96.9482 OP941213.1 Candidatus Borrelia caatinga clone PCST 16S ribosomal RNA gene
96.9295 MN304842.1 Uncultured Borrelia sp. clone T15 16S ribosomal RNA gene
96.8414 MT482696.1 Uncultured Borrelia sp. clone 18GG3 16S ribosomal RNA gene
96.7547 MT013213.1 Uncultured Borrelia sp. clone OrietCE 16S ribosomal RNA gene
96.7504 LC741324.1 Borrelia sp. MTNP-32 gene for 16S ribosomal RNA
96.6929 AB111850.1 Borrelia turcica gene for 16S rRNA
96.6667 MK453304.1 Uncultured Borrelia sp. clone PK37 16S ribosomal RNA gene
96.6596 MT013214.1 Uncultured Borrelia sp. clone TabajaraCE 16S ribosomal RNA gene
96.6553 OQ725662.1 Uncultured Borrelia sp. clone 54_16S 16S ribosomal RNA gene
96.6518 MT013210.1 Uncultured Borrelia sp. clone JericoCE 16S ribosomal RNA gene
96.6491 U42284.1 Borrelia anserina 16S ribosomal RNA gene
96.6469 MW889882.1 Borrelia sp. A126 16S ribosomal RNA gene
96.6317 MK453305.1 Uncultured Borrelia sp. clone STN357 16S ribosomal RNA gene
96.6230 OR058600.1 Uncultured Borrelia sp. clone SSK31 16S ribosomal RNA gene
96.6193 KU308247.1 Uncultured Borrelia sp. clone Ticino01_2015 16S ribosomal RNA gene
96.6027 LC741327.1 Borrelia sp. SLNP-13 gene for 16S ribosomal RNA
96.5986 OP081026.1 Uncultured Borrelia sp. clone 24T 16S ribosomal RNA gene
96.5695 MG452684.1 Borrelia sp. isolate Bsp_Tick14 16S ribosomal RNA gene
96.5485 KY563158.1 Borreliella burgdorferi isolate 11-326 16S ribosomal RNA gene
96.5333 NR_114544.1 Borrelia coriaceae strain Co53 16S ribosomal RNA
96.5089 AF228031.1 Borrelia hermsii strain SB82 16S ribosomal RNA gene
96.5077 AB897891.1 Uncultured Borrelia sp. gene for 16S ribosomal RNA
96.5077 AB529427.1 Borrelia sp. TA2 gene for 16S rRNA
96.4983 MK367715.1 Borrelia caucasica strain CHICH-D 16S ribosomal RNA gene
96.4789 PP729468.1 Uncultured Borrelia sp. clone mimona1 16S ribosomal RNA gene
96.4623 KX171919.1 Borrelia hermsii isolate YBT-21 16S ribosomal RNA gene
96.3636 MK367713.1 Borrelia caucasica strain INH 16S ribosomal RNA gene
96.3504 KU954115.1 Borrelia sp. NL230 16S ribosomal RNA gene
96.3122 MG004679.1 Borrelia sp. isolate Bsp_Tick2 16S ribosomal RNA gene
96.3023 KT364299.1 Borrelia sp. 1939 16S ribosomal RNA gene
96.2963 MK367714.1 Borrelia caucasica strain CHICH-C 16S ribosomal RNA gene
96.2391 LC164122.1 Borrelia miyamotoi gene for 16S rRNA
96.2194 ON365960.1 Uncultured Borrelia sp. clone BJ164 16S ribosomal RNA gene
96.1590 M60968.1 B.hermsii 16S ribosomal RNA
96.1370 MW301926.1 Borrelia sp. isolate BE5 16S ribosomal RNA gene
96.1356 KT364339.1 Candidatus Borrelia africana strain TCI22 16S ribosomal RNA gene
96.1240 PV826772.1 Uncultured Borrelia sp. clone CRETAV-OMAS069 16S ribosomal RNA gene
96.1030 M64312.1 B.anserina 16S ribosomal RNA
96.0595 MK453306.1 Uncultured Borrelia sp. clone HKK19 16S ribosomal RNA gene
96.0568 KT364341.1 Candidatus Borrelia ivorensis strain TCI351 16S ribosomal RNA gene
96.0526 M60970.1 B.coriaceae 16S ribosomal RNA
96.0259 PP230821.1 Uncultured Borrelia sp. clone 78_bov 16S ribosomal RNA gene
95.9970 ON365959.1 Borrelia miyamotoi 16S ribosomal RNA gene
95.9945 M72397.1 Borrelia anserina 16S small subunit ribosomal RNA
95.9742 KT364305.1 Borrelia sp. 2354 16S ribosomal RNA gene
95.9710 KT722787.1 Borrelia sp. TVY 14.022 16S ribosomal RNA gene
95.9184 KY563202.1 Borreliella burgdorferi isolate A13-477 16S ribosomal RNA gene
95.9034 NR_025861.1 Borrelia miyamotoi strain HT31 16S ribosomal RNA
95.8604 AY682921.1 Borrelia lonestari isolate MO2002-V2 16S ribosomal RNA gene
95.7117 OR878665.1 Uncultured Borrelia sp. clone ML58 16S ribosomal RNA gene
95.6355 KU196080.1 Borrelia miyamotoi strain Sonom53 16S ribosomal RNA gene
95.5269 MW301940.1 Borrelia miyamotoi isolate 188 16S ribosomal RNA gene
95.5076 OP081024.1 Uncultured Borrelia sp. clone 1T 16S ribosomal RNA gene
95.3265 U28502.1 Borrelia sp. 16S ribosomal RNA gene
95.2859 PQ488732.1 Uncultured Borrelia sp. clone ACGMP001-5 16S ribosomal RNA gene
95.1569 U28503.1 Borrelia duttonii 16S ribosomal RNA gene
95.1296 AH003459.2 Borrelia hermsii strain M1001 16S ribosomal RNA (16S rRNA)
95.0450 OP081025.1 Uncultured Borrelia sp. clone 22T 16S ribosomal RNA gene
94.8223 PQ488741.1 Uncultured Borrelia sp. clone ACRED011-60 16S ribosomal RNA gene
94.7802 KY563151.1 Borreliella americana isolate 12-40 16S ribosomal RNA gene
94.7186 AY626138.1 Borrelia sp. R57 16S ribosomal RNA gene
94.7085 MW301930.1 Borrelia miyamotoi isolate 6 16S ribosomal RNA gene
94.5338 KF957672.1 Borrelia sp. CA684 16S ribosomal RNA gene
93.7845 U28418.1 Borrelia crocidurae 16S ribosomal RNA gene
86.4989 U28500.1 Borrelia burgdorferi strain Rioja (garinii) 16S ribosomal RNA gene
84.2023 PQ508352.1 Uncultured Borrelia sp. clone Bor-ASV1 16S ribosomal RNA gene
47.1837 JX888452.1 Borrelia afzelii isolate zy 16S ribosomal RNA gene
46.7178 AF497996.1 Borrelia spielmani 16S ribosomal RNA gene

So if B. burgdorferi was created from B. anserina by Traub, then were all of the other species of Borrelia in the LB group also created from B. anserina by Traub?

A 1% divergence in the 16S gene is considered to typically correspond to about 50 million years of evolution in free-living bacteria, or about 1-2 million years in endosymbionts. [https://www.pnas.org/doi/full/10.1073/pnas.96.22.12638] Pathogenic bacteria often have a rate of evolution that is intermediate between free-living bacteria and endosymbionts, even though I don't know if that's the case for Borrelia. But regardless, a 4% divergence in 16S between species of Borrelia would likely correspond to tens or hundreds of millions of years of evolution.

So did Traub find some way to accelerate evolution by around 7 to 8 orders of magnitude, so that within a period of only a few years, he was able to create all the different species in the LB group by serial passage starting from Borrelia anserina?

In the introduction to Finnegan's book, Loftus suggested that Borrelia burgdorferi was created through serial passage, and he wrote that "serial passages can achieve laboratory viral and bacterial mutations in a few weeks that would take decades to develop in nature". [https://play.google.com/books/reader?id=aTKdEQAAQBAJ&pg=GBS.PT11.w.0.4.13_207] But the difference between decades and a few weeks is only about 2 to 3 orders of magnitude, and not 7 to 8 orders of magnitude.

The term Borrelia burgdorferi is sometimes employed in a broad sense (sensu lato), which refers to a group of species of Borrelia associated with Lyme borreliosis, but the term is more often employed in a strict sense (sensu stricto), which only includes a single species within the group. The broad sense is synonymous with the LB group of Borrelia species.

A study from 2024 said that the "mean age of the last common ancestor of all Bbsl species is estimated to be 117 ± 58 million years (Myr)" (where "Bbsl" is short for Borrelia burgdorferi sensu lato, which does not include Borrelia anserina). [https://journals.asm.org/doi/10.1128/mbio.01749-24]

In one study the most recent common ancestor of North American strains of Borrelia burgdorferi sensu stricto was dated to about 60,000 years ago. [https://pmc.ncbi.nlm.nih.gov/articles/PMC6431794/] So it's not possible for the strains to be descended from a single ancestral strain that was created less than a hundred years ago by Erich Traub.

Kathleen Dickson on Borrelia anserina

In his book Finnegan wrote: "Kathleen Dickson of TruthCures was the first to make this connection between Borrelia burgdorferi and Borrelia anserina, so that credit belongs to her, see: Dickson, K. 'CRIMINAL CHARGE SHEETS JUNE 2017 Lobbying for a Hearing for Referral to the USDOJ for a Prosecution of the Lyme Disease Crimes.' 2017. Published at: https://docs.wixstatic.com/ugd/47b066_01d68b1309ae457b81df1e06e6beaele.pdf, However, I am adding to her discovery by now showing it was in Traub's possession and the agent was then in his possession and he used very original means to adapt it to new hosts before the advent of modern genetic engineering." The PDF he linked had been deleted, and I didn't find the article by googling for its title. I didn't find anything by googling for site:truthcures.org anserina either, but I found a couple of posts about Borrelia anserina from Kathleen Dickson's Facebook group. [https://www.facebook.com/groups/271420453060565/search/?q=anserina] In one post she wrote "The new Plum Island borrelia related to African bird Relapsing Fever (anserina) ? Yeah, it's its closest relative says the NIH." But Borrelia burgdorferi sensu stricto is much closer to other species in the LB group than to Borrelia anserina, so she may have meant that the RF group which includes Borrelia anserina is the closest neighbor of Borrelia burgdorferi sensu lato (but even that is not correct, because species of Borrelia that infect reptiles are closer to the LB group than the RF group is):

But still, the tMRCA of the LB and RF groups is probably greater than the tMRCA of humans and chimps, and just because chimps happen to be the closest neighbor species of humans, humans cannot have been created by Nazis from chimps less than a hundred years ago.

Shared flagellar epitopes

Later in the book Finnegan wrote:

Much later, we can see that the Lyme Disease spirochete was in fact related to the avian spirochete when comparing DNA from the flagella[D] of the spirochete. It was published in a 1989 paper "Shared Flagellar Epitopes of Borrelia burgdorferi and Borrelia anserina."[82] Furthermore, striking relationships were likewise shown in a 1995 paper "A Morphological Characterization of Borrelia anserina"[83] Borrelia burgdorferi, Borrelia garinii, and Borrelia afzelii, are the three species of Borrelia spirochetes known to produce Lyme Disease, and these are most closely related to the parent strain Borrelia anserina. This was reflected in several additional publications.[84, 85] Furthermore, the Lyme disease spirochete is maintained and carried by many different birds, further proving the Lyme disease spirochete came from Borrelia anserina.[86]

When I asked Grok if what Finnegan wrote was true, Grok said:

No, the statement is not true. It overstates the evidence on the relationship between Borrelia burgdorferi (the main Lyme disease agent) and Borrelia anserina (an avian relapsing fever spirochete).

The 1989 paper by Walker et al. shows shared flagellar epitopes between B. burgdorferi and B. anserina, reflecting conserved flagellin proteins common across spirochetes. This indicates antigenic cross-reactivity due to distant common ancestry at the genus level, not close phylogenetic ties or derivation of one from the other.

The 1995 paper by Hovind-Hougen describes the morphology of B. anserina but makes no phylogenetic comparison to Lyme agents (B. burgdorferi, B. garinii, B. afzelii) and does not suggest they are closely related.

Modern phylogenetics (using 16S rRNA, flaB, multilocus typing, and genomes) places the Lyme borreliosis (LB) group in one monophyletic clade and the relapsing fever group (RFG, including B. anserina) in a separate sister clade. B. anserina belongs firmly to the RFG (soft-tick transmitted, avian-specific) and is not basal to or the "parent" of the LB group. Hard-tick species like B. miyamotoi are closer to LB than B. anserina.

The cited papers 84 and 85 do not support a close relationship. Marconi et al. (1995) analyzes divergence within Lyme-related borreliae and mentions no B. anserina. Fukunaga et al. (1996) uses flaB sequences to separate Lyme borreliae from relapsing fever/avian species like B. anserina, reinforcing distinct lineages.

Birds serving as reservoirs for B. burgdorferi (via hard ticks like Ixodes) reflects ecological overlap, not evolutionary origin from B. anserina (soft-tick transmitted fowl spirochetosis agent). No credible evidence positions B. anserina as the closest relative or ancestor of Lyme disease agents.

Plot for 16S distance to anserina and burgdorferi

In the next plot I calculated a 16S distance matrix the same way as earlier, but I now visualized the results in a format where the x-axis shows distance to the B31 reference genome of Borrelia burgdorferi sensu strictu, and the y-axis shows distance to one Borrelia anserina sequence I picked at random. Apart from the sequence with an x-axis value of zero, all other sequences labeled burgdorferi are only sensu lato and not sensu stricto, because I thinned out the distance matrix to remove sequences that had less than 0.4% distance to any previous sequence in the matrix, which filtered out all other sensu stricto sequences.

The colored groups are based on a clustering analysis where similar sequences are grouped together. You can see that there are 5 different clusters in the LB group, so it would've been impossible for all 5 clusters to have emerged in the past 100 years.

Using the common rule of thumb for free-living bacteria, each 1% step in the plot would represent 50 million years of evolution, so the distance between the anserina and burgdorferi sensu stricto sequences would be about 4 times 50 million years, or about 200 million years. The Borrelia genus might have a slightly faster rate of evolution than typical free-living bacteria, but the rate is still many orders of magnitude too slow for all of the LB species to have emerged from anserina within the past 100 years. And anserina isn't even the closest neighbor of the LB group within the RF group:

m=100-read.table("https://sars2.net/f/borre.pid.tsv.gz",sep="\t",header=T,row.names=1,check=F)

xpop=grep("B31",rownames(m),value=T)[1]
ypop=grep("M64312.1 B.anserina 16S ribosomal RNA",rownames(m),value=T)[1]

pick=m[,ypop]<6&m[,xpop]<6
m=m[pick,pick]

pick=rowSums(lower.tri(m)&m<.4)==0
m=m[pick,pick]

name=sub("16S.*","",sub("^.*? ","",rownames(m)))
name=gsub("(isolate|strain|partial|Uncultured|Borrelia|Borreliella|gene for|DNA for|sp\\.)"," ",name)
name=gsub("^ *| *$","",name)
name=gsub("  *"," ",name)

p=data.frame(x=m[,xpop],y=m[,ypop])
seg=cbind(p[rep(1:nrow(p),each=2),],p[apply(m,1,\(x)order(x)[2:3]),])|>"colnames<-"(paste0("V",1:4))

lims=max(p)*c(-.03,1.02)

nk=16;k=factor(cutree(hclust(as.dist(m)),nk))
hue=c(0,21,10,6,30,16,3,25)*10+15
set.seed(0)
color=c(hcl(hue,110,60),hcl(hue,70,80))[sample(nlevels(k))]

xtit="Borrelia burgdorferi sensu stricto (B31) (AF467957)"
ytit="Borrelia anserina (M64312)"

ggplot(p,aes(x,y))+
geom_vline(xintercept=0,color="gray50",linewidth=.3)+
geom_hline(yintercept=0,color="gray50",linewidth=.3)+
geom_abline(linetype="dashed",color="gray50",linewidth=.3)+
ggforce::geom_mark_hull(aes(color=k,fill=k),concavity=1000,radius=unit(.3,"lines"),expand=unit(.3,"lines"),alpha=.15,size=.15)+
geom_segment(data=seg,aes(x=V1,y=V2,xend=V3,yend=V4),color="black",linewidth=.15)+
geom_point(aes(color=k),size=.5)+
ggrepel::geom_text_repel(data=cbind(p,name),aes(color=k,label=name),size=2,max.overlaps=Inf,segment.size=.2,min.segment.length=.2,force=10,force_pull=2,box.padding=.13)+
labs(title="Distance percent in 16S ribosomal RNA gene",subtitle=paste0("The colored clusters are based on cutting a hierarchical clustering tree at the height where it has ",nk," subtrees. Each point is connected with a line to its two closest neighbors. Positions where either sequence has a gap are not counted.")|>stringr::str_wrap(80),x=paste0("Distance to ",xtit),y=paste0("Distance to ",ytit))+
scale_x_continuous(limits=lims,breaks=0:10,labels=\(x)paste0(x,"%"))+
scale_y_continuous(limits=lims,breaks=0:10,labels=\(x)paste0(x,"%"))+
scale_fill_manual(values=color)+
scale_color_manual(values=color)+
coord_fixed(clip="off",expand=F)+
theme(axis.text=element_text(size=8,color="gray80"),
  axis.text.x=element_text(margin=margin(4)),
  axis.text.y=element_text(angle=90,vjust=1,hjust=.5),
  axis.ticks=element_line(linewidth=.3,color="gray50"),
  axis.ticks.length=unit(-5,"pt"),
  axis.title=element_text(size=9,color="white"),
  legend.position="none",
  panel.background=element_rect(fill="gray30"),
  plot.background=element_rect(fill="#444",color=NA),
  panel.grid=element_blank(),
  plot.subtitle=element_text(size=8,color="white",hjust=.5),
  plot.title=element_text(size=10,color="white",hjust=.5,margin=margin(1,,4)))
ggsave("1.png",width=7,height=7,dpi=300*4)
system("magick 1.png -resize 25% -trim -bordercolor \\#444 -border 24 -dither none -colors 256 1.png")

In my plot Tick98M is approximately equally close to Bbss and anserina but slightly closer to Bbss. Tick98M is part of a group of Borrelia species that infects reptiles and echidnas, which is called REP and which was first described in a paper titled "Isolation and characterization of a novel Borrelia group of tick-borne borreliae from imported reptiles and their associated ticks". [https://www.ncbi.nlm.nih.gov/nuccore/AB473531.1, https://enviromicro-journals.onlinelibrary.wiley.com/doi/10.1111/j.1462-2920.2009.02054.x] The REP group is probably closer to the LB group on average than the RF group is.

Similarity percent in flagellin gene

Finnegan posted the table below from a paper from 1996, where the top row shows the similarity percent of the flagellin gene to B31, which is the common reference strain of Borrelia burgdorferi sensu stricto. [https://x.com/AWFinnegan/status/1905407120415088920, https://www.microbiologyresearch.org/content/journal/ijsem/10.1099/00207713-46-4-898] All species within the LB group have an identity percent above 90%, but outside the LB group the highest identity percent is about 84.2% in B. anserina:

A typical rate of mutation for bacterial protein-coding genes like flagellin is about 1e-8 to 1e-9 substitutions per site per year, so a 1% change in the gene would take about 1 million to 10 million years, if you assume no backmutations. A 1% divergence between two different strains evolving in different directions from a common ancestor would take about half of the time, if you assume no backmutations and that the strains don't acquire the same mutations independently.

I downloaded 938 complete chromosome sequences of Borrelia by searching GenBank for (borrelia OR borreliella) 800000:1000000[slen]. [https://www.ncbi.nlm.nih.gov/nuccore/?term=%28borrelia+OR+borreliella%29+800000%3A1000000%5Bslen%5D] When I compared the flagellin gene of the B31 reference genome against the other sequences, the highest identity percent outside the LB group was about 85.6% to a strain of anserina. But there was also about 85% identity to sequences of puertoricensis, fainii, venezuelensis, hermsii, turcicatae, nietonii, tillae, and parkeri (some of which are not shown below, because in order to reduce clutter, I kept only one instance of each unique flagellin sequence):

curl ftp://ftp.ncbi.nlm.nih.gov/entrez/entrezdirect/install-edirect.sh|sh
brew install blast seqkit mafft
curl 'https://eutils.ncbi.nlm.nih.gov/entrez/eutils/efetch.fcgi?db=nuccore&rettype=fasta&id=X15661'>b31flagellin.fa
esearch -db nuccore -query '(borrelia[organism] OR borreliella[organism]) 800000:1000000[slen]'|efetch -format fasta>borrefull.fa
makeblastdb -dbtype nucl -in borrefull.fa
<b31flagellin.fa blastn -db borrefull.fa -outfmt '6 stitle sseq' -max_target_seqs 10000|seqkit tab2fx>flagellin.fa
seqkit grep -nrp B31 flagellin.fa|cat - flagellin.fa|seqkit rmdup -s|mafft --thread 7 --quiet -|seqkit fx2tab|awk -F\\t 'NR==1{split($2,a,"");l=length(a)}{split($2,b,"");d=0;for(i=1;i<=l;i++)d+=a[i]!=b[i];print 100*(1-d/l),$1}' OFMT=%.2f|sort -rn|cut -d, -f1|sed 's/ chromosome.*//'|awk '$1<94'

The output shows the identity percent to B31 for all unique sequences with less than 94% identity to B31, where you can see there's a big gap between the LB sequences with over 90% identity and non-LB sequences with less than 90% identity:

93.94 CP075236.1 Borreliella bavariensis strain JANAGAM1353
93.84 CP075244.1 Borreliella bavariensis strain JAASAAM1091
93.16 CP135180.1 Borreliella sinica strain CMN3
85.63 CP073130.1 Borrelia anserina strain BA2
85.14 CP149102.1 Borrelia puertoricensis strain CAU1
85.14 CP028884.1 Borrelia turcica IST7
85.14 AP027070.1 Candidatus Borrelia fainii Qtaro DNA
85.04 CP138334.1 Borrelia sp. MN22-0132
85.04 CP073220.1 Borrelia venezuelensis strain RMA01
84.95 NZ_CP005680.1 Borrelia hermsii MTW
84.95 CP084623.1 Borrelia hermsii strain ML2
84.95 CP073176.1 Borrelia turicatae 91E135
84.85 CP129306.1 Borrelia turicatae strain BTCAM1
84.75 CP161006.1 Borrelia hermsii strain HSI-sero26
84.65 CP073159.1 Borrelia parkeri strain SLO
84.56 CP043682.1 Borrelia sp. A-FGy1
84.26 NZ_LN609267.1 Borrelia crocidurae strain 03-02
84.16 NZ_CP005706.1 Borrelia hermsii YBT
84.16 NZ_CP004267.1 Borrelia crocidurae DOU
84.07 NZ_AZIT01000001.1 Borrelia duttonii CR2A Contig0001
84.07 NC_011229.1 Borrelia duttonii Ly
84.07 CM146346.1 Borrelia tillae strain Krampitz
83.97 CP169960.1 Borrelia recurrentis strain PBeK
83.87 AP024400.1 Borrelia miyamotoi Y14T18 DNA
83.77 CP075076.1 Borrelia coriaceae strain Co53
83.68 CP072479.1 Borrelia miyamotoi strain LB-2001
83.58 CP021872.1 Borrelia miyamotoi strain CA17-2241
83.58 AP024372.1 Borrelia miyamotoi HT24 DNA
83.28 CP181375.1 Candidatus Borreliella tachyglossi strain G246
83.19 CP025785.1 Candidatus Borreliella tachyglossi strain Bc-F10-1268
82.99 FV536056.1 Modified Microbial Nucleic Acid
82.89 CP088943.1 Borrelia sp. RT1S
82.89 AP024401.1 Borrelia sp. HM DNA
82.80 CP088936.1 Borrelia sp. RT5S
82.50 CP075444.1 Borreliella afzelii strain PJe

TICK98M and many other samples in the reptile-echidna group are not included above, because they were missing a full chromosome sequence and I extracted the flagellin sequences from the full chromosome sequence.

My identity percentages are slightly different from the percentages in the paper from 1996, because I looked at the full flagellin gene but the paper from 1996 looked at fragments of the gene with a length of about 200 to 500 bases.

But anyway, the question of whether anserina has the closest flagellin gene to B31 or not doesn't make a difference to the validity of Finnegan's theory, because it's completely impossible for Erich Traub to have mutated the flagellin gene by 14% through serial passage within a time span of a few years.

Similarity plot for whole chromosome

I told Finnegan on Twitter that the 16S distance between anserina and burgdorferi corresponds to a tMRCA of about 200 million years. [https://x.com/henjin256/status/2036272443992445130] He blocked me without replying to me, but a few hours later he tweeted about a paper that demonstrated that bacteria could acquire a 16S gene from another species of bacteria through horizontal gene transfer, so he seems to have suggested that horizontal gene transfer might explain the divergence between the 16S genes of anserina and burgdorferi: [https://x.com/AWFinnegan/status/2036496401706684835, https://pmc.ncbi.nlm.nih.gov/articles/PMC3661144/]

However a problem with his explanation is that anserina and burgdorferi are not only divergent in the 16S gene but also in other parts of the genome, and there's a fairly stable similarity level of about 75% throughout the chromosome:

# curl 'https://eutils.ncbi.nlm.nih.gov/entrez/eutils/efetch.fcgi?db=nuccore&rettype=fasta_cds_na&id='{NZ_CP073130.1,NZ_CP019767.1}|mafft --thread 7 ->borre.fa

t=as.matrix(Biostrings::readAAStringSet("borre.fa"))

ref=t[grep("burg",rownames(t)),]
targ=grep("burg",rownames(t),value=T)

gene=fread("name,start,end,height
Flagellin,147648,148658,1
16S,443773,445308,1")

pos=seq_along(ref)+cumsum(ref=="-")
gene$start=pos[gene$start]
gene$end=pos[gene$end]

window=1000;step=200

t1=t[rownames(t)!=targ,,drop=F]
t2=t[targ,,drop=F]
ncol=ncol(t)
starts=seq(1,ncol,step)

sim=apply(t1,1,\(seq)sapply(starts,\(i){start=max(1,i-window%/%2);end=min(ncol,i+window%/%2)
  mean((seq[start:end]==t2[start:end])[seq[start:end]!="-"&t2[start:end]!="-"]) # ignore gaps
  # mean(seq[start:end]==t2[start:end]) # don't ignore gaps
}))

p=na.omit(data.table(x=starts[row(sim)],y=100*c(sim),z=colnames(sim)[col(sim)]))
p[,z:=factor(z,p[,mean(y),z][order(-V1),z])]

hue=c(0,210,120,60,300,160,30,250)+15
color=c(hcl(hue[1:3],130,55),"black",hcl(hue[4:5],130,55),"gray50",hcl(hue,100,30),"gray20")[1:nlevels(p$z)]

ystart=0;yend=100;ystep=10;xstart=0;xend=max(p$x);xstep=1e5

ggplot(p)+
geom_vline(xintercept=xbreak,color="gray88",linewidth=.4)+
geom_hline(yintercept=seq(ystart,yend,ystep),color="gray88",linewidth=.4)+
annotate("rect",xmin=xstart,xmax=xend,ymin=ystart,ymax=yend,lineend="square",linejoin="mitre",fill=NA,color="gray88",linewidth=.4)+
geom_line(aes(x,y),linewidth=.5)+
geom_rect(data=gene,aes(xmin=start,xmax=end,ymin=ystart+(height-1)*annoh*(yend-ystart),ymax=yend),fill="#ff4444",linewidth=0)+
geom_text(data=gene,vjust=0,aes(x=rowMeans(cbind(start,end)),label=paste0(name,"\n(",start,"-",end,")"),y=ystart+(yend-ystart)*.05),size=3.5,lineheight=.9,color="#ff4444")+
labs(title="Similarity between Borrelia burgdorferi and Borrelia anserina",subtitle=paste0("Step ",step,", window ",window,". Positions with gaps are ignored.\nAccessions NZ_CP019767 (B31) and NZ_CP073130 (BA2)."))+
scale_x_continuous(limits=c(0,xend),breaks=xbreak,position="top",labels=\(x)ifelse(x>=1e3,paste0(x/1e3,"k"),x))+
scale_y_continuous(limits=c(ystart,yend),breaks=seq(ystart,100,ystep),labels=\(x)paste0(x,"%"))+
coord_cartesian(clip="off",expand=F)+
scale_color_manual(values=color)+
theme(axis.text=element_text(size=11,color="gray40"),
  axis.ticks=element_line(linewidth=.4,color="gray87"),
  axis.ticks.length=unit(3,"pt"),
  axis.title=element_blank(),
  legend.position="none",
  panel.background=element_blank(),
  panel.grid=element_blank(),
  plot.margin=margin(5,16,10,5),
  plot.subtitle=element_text(size=11,hjust=.5,margin=margin(,,3)),
  plot.title=element_text(size=11,face=2,hjust=.5,margin=margin(,,4)))
ggsave("1.png",width=6,height=4,dpi=300*4)
system("magick 1.png -resize 25% -colors 256 1.png")

The divergence time t can be calculated as t=K/μ/2, where K is the number of substitutions per site with Jukes-Cantor correction, and μ is the rate of substitutions per site per year. In one paper the mutation rate of Borrelia burgdorferi was estimated to be on the order of 1e−9 substitutions per site per year. [https://www.pnas.org/doi/10.1073/pnas.0903810106] The K parameter for a similarity percent of 75% is -3/4*ln(1-4/3*(1-.75)), which is about 0.304, and 0.304/1e-9/2 gives a divergence time of about 150 million years.

Traub's connection to Plum Island

Traub may have moved back to Germany before USDA scientists started to work on Plum Island

In his book Finnegan wrote: "That same year [1956], another conference was held, this time at Plum Island Animal Disease Center (PIADC) for its opening day ceremony, with Dr. Erich Traub as one of the guests at this conference for Plum Island.[33] Michael Carroll previously described the events in his Plum Island exposé.[34] This was one of many instances where Traub, confessed Soviet double agent, was allowed back on American soil to attend symposiums and events at the USDA." Footnote 33 was: "'Proceedings of Symposium on Vesicular Diseases: Plum Island Animal Disease Laboratory September 27-28, 1956 : Symposium on Vesicular Diseases (1957 : Plum Island, N.Y.).' 1970. Internet Archive. [Washington, D.C.] : Agricultural Research Service, U.S. Dept. of Agriculture. January 1, 1970. https://archive.org/details/CAT31325716/page/40". The document he linked doesn't actually mention Traub attending the event, so I don't know if Finnegan relied on Lab 257 as a source that Traub attended the event. The opening day ceremony refers to the opening of PIADC and Building 101 which was the main laboratory building of PIADC.

A history of PIADC says: "In 1952, the Army decided to suspend operations at Fort Terry and to transfer Plum Island to USDA's Bureau of Animal Industries. USDA scientists moved to the renovated Building 257 in 1953. Building of a new facility, to be known as Building 101, started on July 1, 1954, and the building was dedicated on September 26, 1956. The Plum Island Animal Disease Center (PIADC) was inaugurated; it occupied the new building, and the 18 Fort Terry-era buildings were renovated by the Army." [https://www.nationalacademies.org/read/13454/chapter/11]

Erich Traub moved back to Germany in 1953, but I don't know if he had already moved to Germany by the time USDA scientists moved to Building 257 in 1953.

In his book Finnegan wrote: "Traub was in Bogotá, Colombia periodically until the end of 1952, and returned to Maryland, and soon decisions were made for Traub to return to Germany on October 7, 1952, to lead a virus research institute in Tübingen, West Germany. Therefore, Erich Traub submitted his resignation from the position with the U.S. military, but continued research for them in Tübingen.[25,26] Traub set himself up at the University of Tübingen upon his return, which became the cover story for those not 'in the know' about Traub's real purpose for leaving America. Outsiders would be told that the scientist just decided to pack up and go home.[27] Traub's repatriation was approved and on January 14, 1953, Traub and his family boarded the SS Stockholm, and sailed back to Germany, where he began his position at the University of Tübingen's Federal Research Institute for Virus Disease of Animals (Bundesforschungsanstalt fur Viruskrankheiten).[28]" Footnote 27 refers to personal communication with Loftus and footnotes 25 and 28 refer to Traub's JIOA file.

A paper published in the Long Island History Journal said: "Plans for an animal research facility at Plum Island began in 1952 when Fort Terry was transferred to the U.S. Army Chemical Corps. Turning the Fort into such a facility required the remodeling of eighteen buildings, which was only partially completed by May 1954. The laboratory, however, was deactivated even before opening its doors. This was not a complete loss due to the fact that the United States Department of Agriculture (USDA) was already planning to build a new facility to study foot and mouth disease, a contagious viral disease of cattle and swine known for fever and blisters around the mouth and hooves. Congress was urged to do this after numerous outbreaks of this contagious disease in Mexico in 1946, and in Canada in 1952. The new USDA facility was completed in June 1954." [https://dspace.sunyconnect.suny.edu/server/api/core/bitstreams/2adfd9d3-f654-4c29-b11a-c214a7e37e31/content] I don't know what it meant by the laboratory being "deactivated".

One of the main reasons why Finnegan and Carroll speculated that Traub was connected to Plum Island was that Traub was employed by the USDA, which operated the Plum Island Animal Disease Center. But in fact USDA scientists may have begun to work at PIADC only after Traub had already moved out of the United States.

Three visits to Plum Island

In the first chapter of Lab 257 Carroll wrote: "Traub can be physically placed on Plum Island at least three times - on dedication day in 1956 and two visits, once in 1957 and again in the spring of 1958."

It's difficult to tell which of the sources in Carroll's bibliography backed up the claim that Traub visited Plum Island three times, apart from an undated memo titled "Proposed Visit to Plum Island by Dr. Erich Traub". But in the bibliography for the first chapter, there were only four sources dated 1956 or later:

I didn't find any of the sources published online.

In his book Finnegan wrote: "Traub was then approved for several trips to re-enter the United States to take part in symposiums and conferences in the field of virology and agriculture and be a guest of honor at Plum Island's opening day ceremony in 1956.[7,8] According to the travel logbook used by the Tübingen Institute, in spring of 1953, Traub and several colleagues from the Institute took a trip to Basel, Switzerland to visit a Swiss veterinary institute.[9] In June of that year, Werner Schäfer and his colleague Otto Armbruster, who were working with Traub from the Max Planck Institute at the time, took a trip for Traub to Berlin, East Germany to visit the Siemens and Halske, Co., the company in charge of the electron microscope department at Insel Riems and the University of Berlin.[10] The following month, Traub traveled to Rome and to Austria for the FAO, to attend a conference on Foot-and-Mouth Disease.[11]"

Footnote 7 was: "Traub, E. Specific Immunity as a factor in the Ecology of Animal Viruses. Perspectives of Virology: A Symposium. John Wiley & Sons, Inc. New York: Chapman and Hall. Ltd., London; pp. 160-183. (1959)". Footnote 8 was: "USDA, Plum Island Animal Disease Center (PIADC). Memorandum 'Proposed Visit to Plum Island by Dr. Erich Traub,' from R. A. Carlson, Administrative Officer, ARS, to M. S. Shahan, Director, Plum Island Animal Disease Laboratory, undated" (which was the exact same citation as given in Lab 257, so I don't know if Finnegan saw the actual document, or if he just copied the citation from Carroll's bibliography). Footnotes 9-11 were: "Bundesforschungsanstalt für Viruskrankheiten der Tier, [travel records activity]. [Investigations against members of the Federal Research Center for Virus Diseases in Animals: Government official Hans Friedrich Melz and President Prof. Dr. Erich Traub], 1958 - 1963. (August 12, 1958). B 116/33791-B/116-33793. Bundesarchiv, Koblenz." I didn't find any of the documents posted online.

Why didn't Finnegan cite the German "travel records activity" documents as evidence for the supposed trips to the United States in 1956, 1957, and 1958? The citation he gave for the documents seems to refer to a series of 3 documents from the years 1958 to 1963, where August 1958 looks like the date of the first document. But if the documents mentioned a trip in 1953, then they would probably also cover the years 1956-1958. Finnegan didn't specify if trips to the United States were mentioned in the German documents or not.

Carroll said that Traub's third visit to Plum Island took place in the spring of 1958, but transatlantic passenger jet flights only began in October 1958. [https://en.wikipedia.org/wiki/Transatlantic_flight] A trip across the Atlantic on a ship took around 7-9 days. So if Traub took three return trips to the United States by ship in 1956-1958, he would've had to spend about 4% of the years 1956-1958 onboard ships on the Atlantic.

It would've been a pain in the ass to spend 14-18 days onboard a ship just so you could attend the opening ceremony of PIADC, so Traub probably wouldn't have taken the trip unless he had some other business to take care of in America apart from simply attending the ceremony.

Traub does in reality seem to have traveled to the US to attend a virology symposium in 1958. The book about the symposium is available at Anna's Archive, and it describes conversation between Traub and other people who attended the symposium. [https://annas-archive.gl/search?q=%22Perspectives+in+virology%22+1959] But that doesn't necessarily mean that Traub visited Plum Island on the same trip. So far I have not found good evidence that Traub would have ever visited Plum Island.

Finnegan responds to me at Substack

In March 2026 Finnegan posted response to the early comments about his book I had published on my website. [https://awfinnegan.substack.com/p/clarification-on-the-lyme-borreliosis]

Anserina and burgdorferi

Finnegan wrote:

Furthermore, there are elements of this story that no one has ever studied - mainly in the highly sophisticated conditions created by Erich Traub and his German colleagues during WWII, when he began adapting multiple overlapping infections from different sources into the same tick vector like a Russian-doll cocktail, with the addition of bacteriophage varieties (including lyophilized or dry-frozen bacteriophages),[6,7] viruses,[8] and mycoplasma,9 all of which Insel Riems was working with during Traub's tenure as Vice President - overseeing the entire phase of Insel Riems research in the WWII years and well into the beginnings of the Cold War under Soviet occupation. The addition of viruses, phages, and mycoplasma would act as gene shuttles between the different co-infecting agents, allowing for rapid evolution and gene swapping between numerous foreign pathogens that had not been exposed to each other previously. Such controlled environments could greatly accelerate mutation rates, adapt pathogens to many new hosts, change its tropisms, and take on a myriad of new characteristics - making short-term changes appear to be long-term evolutionary distance.

To add another layer of complexity, once these extremely unique and unusual biological specimens were introduced into wild habitats of ecosystems in vastly different parts of the globe by nations duplicating or conducting further biowarfare research and testing activities, it further complicates the theory of natural evolution with yet even more highly divergent and unique conditions from the native viruses and microbes in each specific ecosystem where these vectors are released. This could diversify further what seem like millions of years of evolution when in fact were just a few years of highly exceptional conditions duplicated across varying climatic conditions within a few years in their respective biological warfare programs.

I showed the text above to Grok and asked: "If Borrelia burgdorferi was created by bioweaponeers less than 100 years ago from Borrelia anserina, could conditions like this have caused burgdorferi to have only around 75% nucleotide similarity across the whole chromosome from anserina? Paragraphs-only answer." I got this answer:

No, the conditions described - co-infecting ticks with layered pathogens, bacteriophages, viruses, and mycoplasma as potential gene shuttles under controlled WWII-era bioweapon research - could not have produced a Borrelia burgdorferi chromosome showing only around 75% nucleotide similarity to that of Borrelia anserina in less than a century. Bacterial whole-chromosome average nucleotide identity (ANI) at this level reflects deep evolutionary divergence between the Lyme-associated Borreliella group and the relapsing-fever Borrelia group, a separation that phylogenomic data place millions of years in the past through gradual accumulation of mutations, insertions, deletions, and rearrangements under natural selective pressures. Even aggressive horizontal gene transfer mediated by phages or other mobile elements transfers relatively small genomic segments at a time and cannot wholesale rewrite hundreds of kilobases across an entire linear chromosome while preserving the precise synteny, telomere structure, replication machinery, and host-vector adaptation required for a viable spirochete.

Rapid "gene swapping" in a Russian-doll tick cocktail might accelerate acquisition of a few accessory genes or plasmids from co-infecting microbes, but it cannot generate the genome-wide sequence divergence observed. Achieving 25% nucleotide dissimilarity from a near-identical starting anserina genome would demand either hypermutator-level error rates sustained across thousands of generations without lethal collapse or massive, coordinated replacement of core chromosomal regions with entirely unrelated sequences - neither of which is biologically feasible in laboratory or field release settings spanning mere decades. Natural mutation rates, even elevated under stress or mutagenesis, fall orders of magnitude short of the required changes; phage-mediated transduction and mycoplasma- or virus-assisted shuttling simply lack the capacity to orchestrate such precise, large-scale remodeling without destroying the organism's functionality.

The sophisticated overlapping-infection protocols pioneered by researchers like Erich Traub undoubtedly enabled adaptation to new hosts and vectors, potentially speeding niche shifts or antigenic variation, yet these processes still operate within the constraints of existing genetic mechanisms. They could not compress millions of years of apparent evolutionary distance into a few years of exceptional conditions, nor could subsequent global releases into varied ecosystems retroactively manufacture the consistent phylogenetic distance now measured between the two species. In short, the 75% chromosomal similarity is a signature of ancient natural divergence, not a hallmark of recent bioweapon engineering.

Finnegan also wrote: "As is common in top secret research and development, advances in science were often known many decades before their public disclosures. I believe Insel Riems and the Germans were already up to speed on current modern-day bioengineering back in the days of World War II, as Insel Riems was working with several bacteriophage varieties and Mycoplasma. Both would act to shuttle genes between the different cocktail of pathogens and accelerate rapid evolution." However there is no method even in modern-day bioengineering to accelerate evolution by 6 or 7 orders of magnitude, so you can create a new species of bacteria that is 25% divergent from another species across the whole chromosome within a time span of a few years.

Later Finnegan speculated that Traub might have accelerated evolution through antibiotics: "Traub's work on adapting FMD to chicken eggs showed that antibacterial resistance was an environment Traub was familiar working in when he mentioned that certain bacteria contaminated his FMD experiment and survived heavy doses of Streptomycin and Penicillin, and this may have been done intentionally.[59] He could have adapted Borrelia burgdorferi to such environments making its 16S rRNA operon highly mutable to change, making what seemed like entirely new species and subspecies between the other European and Japanese forms of Lyme disease when in fact it was still an outgrowth of what had started with a single species - Borrelia anserina - in 1939. He would have completely remodeled the spirochete perhaps several times over in his work on high-density pathogen-packed ticks released in variable ecosystems in routine biodefense activities spanning the globe." Some antibiotics like tetracyclines target the ribosome, so they might in fact greatly accelerate the mutation rate of the 16S gene of the ribosome. But it's not only the 16S gene but the whole genome that is divergent between anserina and burgdorferi, and selection for antibiotic resistance would not affect the whole genome but only the parts of the genome that are targeted by the antibiotics. Many species of bacteria have developed antibiotic resistance in the past few decades, but they haven't mutated by 25% throughout the genome and turned into a new species because of antibiotics.

Finnegan also postulated there may have been a "horizontal gene transfer through mycoplasma and bacteriophages to shuttle a sophisticated network of genes between the agents". But then why do burgdorferi and anserina have fairly uniform 75% similarity throughout the genome? If Borrelia burgdorferi had acquired a large region of the chromosome from some other genus of bacteria through horizontal gene transfer, you would be able to do a BLAST search for the region and see that it is closer to the other genus than to Borrelia anserina. But no such region exists.

Studies in serial passage with Kanhai

Finnegan wrote:

Erich Traub had also known that he could use viruses to adapt microorganisms to new species of animals through the formation of heterokaryons. He likely taught this technique to Iranian scientist G. K. Kanhai while in Iran in the late 1960s - teaching him how to change the properties of FMD virus to take on a whole array of new properties, adapt other pathogens to new species and beyond. As Traub said in his collaborative work with Kanhai, just some of the factors he was able to change with ease were:

  1. natural retrogression and termination of epizootics;
  2. increase in potency of the causative agent;
  3. virus adaptation to certain species of animals and escalation or decrease of infectivity and pathogenicity for other species;
  4. different affinity of virus strains for certain cells (cardiac FMD);
  5. differences in susceptibility among individual animals of the same species;
  6. reduced susceptibility in undernourished individuals;
  7. different behavior of different virus types;
  8. persistent infection;
  9. serological variation.[10]

What the paper he linked actually said was that "in the course of this work with cells, observations were made which may have a bearing on certain epidemiological events in the field", which included phenomena like "termination of epizootics" (i.e. ending of an animal disease outbreak): [https://sci-hub.ee/https://onlinelibrary.wiley.com/doi/10.1111/j.1439-0450.1968.tb00327.x]

Traub didn't claim that he had developed a method to end outbreaks of diseases in animals. But he pointed out that serial passage led to a gradual attenuation of the pathogen so eventually it was not able to sustain another passage, which he compared to the natural weakening of a pathogen during a disease outbreak in animals.

Finnegan continued:

Some years later, Kanhai then went on to publish about the use of Sendai virus to adapt the tick-borne disease Theileria parva to a new host via cell-fusion, or the creation of heterokaryons.[10]

The study did not result in T. parva being adapted to hamsters. Grok said:

What it actually demonstrated was a short-term, artificial laboratory trick: using UV-inactivated Sendai virus to force the fusion of T. parva-infected bovine lymphoid cells with uninfected baby hamster kidney (BHK) cells (or mouse cells in related work). This created transient heterokaryons - hybrid cells with mixed bovine and hamster nuclei sharing a common cytoplasm. In these fused cells, the intracellular parasites could be detected for a limited time, sometimes appearing in regions that looked like they contained mostly hamster nuclei.

This was a proof-of-concept for moving a strictly cell-associated parasite across a species barrier in vitro under highly artificial conditions. It did not result in:

Subsequent papers by Irvin, Brown, Kanhai, Stagg and colleagues (e.g., 1975-1976 attempts with mouse Ehrlich ascites tumour cells or further hamster fusions) explicitly explored whether they could generate truly infected, replicating rodent cell lines. These efforts largely failed to produce stable, productive infections; the heterokaryons were short-lived, and the parasites did not establish independent growth in the new cellular environment.

Theileria parva remains highly host-specific to bovines (cattle and African buffalo) under natural conditions. Its schizont stage transforms and replicates inside bovine lymphocytes, and no routine, stable rodent or hamster culture system for T. parva ever emerged from this line of work. The technique was a clever virological tool for studying intracellular parasite behavior in controlled settings, not a method for creating a new, adapted pathogen capable of sustained infection in a different species.

Traub's work at Plum Island

Finnegan wrote: "When Erich Traub was brought to America in Project Paperclip he was brought here and worked with the USDA at Plum Island from the beginning.[26]" Footnote 26 was: "Federal Bureau of Investigation (FBI): RG 65 Erich Traub, (Declassified FBI Investigations on the Loyalties of Erich Traub). NARA., Doc. # QO1-458431291, Doc. # QO1-458431291." He should upload all of these secret intelligence files somewhere. Traub moved to the United States in 1949, but I haven't found evidence that Plum Island was used as a biological research site before 1953 or 1952.

Finnegan wrote: "In one of his applications to return to America in 1958 to attend a conference on virology - long after he had been sent back to Germany in 1952 - he listed an employment position with the Greenport Long Island Station of the Agricultural Research Service (ARS) of the USDA, which is another less common name for Plum Island. He cited the public law 496 80th congress for establishing an FMD lab as his reason for the appointment. So, it can be conclusively stated that he did not just make a few visits to Plum Island, he was very involved in the work done there as an employee from his earlier days in Paperclip.[28] In his Joint Intelligence Objectives Agency (JIOA) file, Traub attended a conference in Washington D. C. in 1950 during his Paperclip tenure and listed B. T. Simms of the USDA as a point of contact if anyone needed to get in touch with him. Simms was a USDA official who was involved in some of the research at Plum Island. We can safely say Traub was working at Plum Island even if initially employed by the U. S. Navy and brought to the Naval Medical Research Institute (NMRI)." When I googled for the term "Greenport Long Island Station" in double quotes, all results for the exact tame came from Finnegan. A history of ARS says: "On November 2, 1953, a Secretary's Memorandum redesignated the Agricultural Research Administration - established in 1942 - as the Agricultural Research Service. This established ARS as USDA's chief scientific research agency." [https://scientificdiscoveries.ars.usda.gov/tellus/stories/articles/agricultural-research-service-history-innovation] Of course it's possible that Finnegan would have worked for the Agricultural Research Administration but he later used its new designation.

However in his book Finnegan specifically wrote that Finnegan worked as an employee of ARS: "A 1958 security investigation by the FBI can place Erich Traub on Plum Island and listed as an employee of the Greenport, Long Island, NY Agricultural Experiment Station, which is Plum Island.[60] He was also at the Beltsville, Maryland Agricultural Experiment Station for the Agricultural Research Service (ARS) of the USDA, working as an employee of the ARS when it was established in 1953, formerly known as the Bureau of Animal Industry (BAI)." But the timeline I quoted above said that ARS was established in November 1953, and Finnegan wrote in his book that Traub had already moved back to Germany in early 1953, and he even visited Switzerland in the spring of 1953. The "Beltsville Agricultural Experiment Station" appears to be an old name for the "Beltsville Agricultural Research Center", which was already established in 1910. [https://agresearchmag.ars.usda.gov/2010/apr/research/, https://www.google.com/search?tbm=bks&q=%22Beltsville+Agricultural+Experiment+Station%22]

Finnegan referred to the 1948 law which authorized the creation of "research laboratories for foot-and-mouth disease and other animal diseases". [https://www.law.cornell.edu/uscode/text/21/113a] But the law didn't specify that a research center should be created specifically at Plum Island, and the process of actually establishing the research center lingered until an outbreak of FMD was detected in Canada in February 1952. [https://www.nationalacademies.org/read/13454/chapter/11] As far as I can tell, renovations of converting Fort Terry to a biological research facility didn't begin until 1952, which would've been towards the end of Traub's stay in the United States in 1949-1953. A history of Plum Island said: "On April 25, 1952, Fort Terry was transferred to the U.S. Army Chemical Corps, which had been planning an animal research laboratory on Plum Island since 1951. The new laboratory was planned to be housed within the Combined Torpedo Storehouse and Cable Tanks (circa 1911), also known as Building 257. Remodeling of 18 Fort Terry buildings was contracted out in 1952." [https://web.archive.org/web/20051103165628/https://usaha.org/news/newsletter/USAHA-Newsletter-Oct2003.pdf]

In Lab 257 Carroll wrote:

USDA engineers and architects armed with magnifying glasses analyzed maps of America's coastline, searching for the right place. Two weeks after the law passed, the USDA found the perfect coastal island: Prudence Island, off the coast of Rhode Island. The USDA had looked at many other sites, including Fort Terry, Plum Island, a surplus island fortress of 840 acres off the east end of Long Island.

Meanwhile, the Army was separately fixing its sights on Fort Terry as a germ warfare island laboratory. At the last minute, it abruptly canceled the surplus sale of the island to Suffolk County and invited the USDA - which watched in horror as wealthy Newporters, after forming the Anti-Prudence Island Laboratory Committee, killed the aggies' plan for nearby Prudence Island - to join them. Debating the need for Plum Island in the U.S. Senate, New York's senators, Irving Ives and Herbert Lehman, demanded that a provision in the law be included to protect the local New York community:

[A]t a location to be selected by the Secretary of Agriculture after full hearings of which reasonable public notice shall be given to those who may reside within twenty-five miles from the island selected. [Italics added]

[...]

As their "reasonable public notice" given, the USDA placed ads in the newspapers one week before the Plum Island hearings.

[...]

Secretary of Agriculture Brannan "selected" Plum Island on July 28, 1952.

The senate hearing only took place in 1952, and the selection of Plum Island in July 1952 took place only about half a year before Traub moved back to Germany.

Newspaper articles about the USDA's plans to set up a laboratory on Plum Island started to appear in July 1952. [https://www.newspapers.com/search/results/?date=1952&keyword=%22plum+island%22+laboratory] But before it a newspaper article from June 25th 1952 said: "Open battle between Long Island and federal authorities threatened yesterday as the Army announced its intentions to use Plum Island as a base for research into germ warfare." [https://www.newspapers.com/article/newsday-nassau-edition/194427451/] At the time even the laboratory by the Army Chemical Corps was still said to be only a proposed laboratory. The article quoted a representative from the Department of Agriculture as saying that "the proposed Army laboratory has no bearing on the Department of Agriculture's decision to study hoof and mouth disease" but that "the defense aspect of the hoof and mouth study was considered important for national defense".

Next a newspaper article from July 1st said: "Two germ-study labs are proposed for the 795-acre islet - one to study only hoof and mouth disease, which the Department of Agriculture wants to erect; and a biological warfare study center, which would be operated by the Army." [https://www.newspapers.com/article/newsday-nassau-edition/194427516/] The article also said: "Before the lab can be built by the Agriculture Department, public hearings must be held by the agricultural committees of both houses and by Secretary of Agriculture Charles Brannan. The provision for hearings was contained in an amendment tacked on to the appropriations bill by Lehman and Ives. A second amendment, also put in by the two New York senators, but cut out by Sen. Kenneth McKellar, (D-Tenn.), chairman of the Senate Appropriations Committee, provided that the governor of the state in which the lab was to be erected would have to give his consent before work could start. The Army's $5,000,000 germ warfare center is subject to neither restriction." But the hearings required by the amendment were only conducted later in July 1952. Perhaps the backup plan was to set up the lab under the auspices of the Army Chemical Corps in case the USDA did not receive a permission to build the lab.

Comment by Roger Breeze to Rachel Verdon

In his blog post Finnegan referred to a quote from Rachel Verdon's book I included on my website. He wrote: "Plum Island was chartered to study not just FMD but all foreign animal diseases that affected poultry, livestock, and man. Rachel Verdon's book Lyme Disease and the SS Elbrus claims that after talking to former Plum Island director Dr. Roger Breeze about whether Plum Island was involved with the Lyme disease outbreaks in America, he adamantly told her it was not true, that they never worked with spirochetes or tick-borne disease, and she believed him.[43] We can see that such a statement is actually a blatant lie - they published a 1961 paper on subclinical Leptospirosis of cattle.[44] Leptospira is a spirochete and Plum Island did work with other tickborne diseases like heartwater (Cowdria ruminantium) and Theileria parva.[45]" Footnote 43 referred to Verdon's book. Footnote 44 was "Siebold, H. R., et al. 'Histopathologic and Serologic Study of Subclinical Leptospirosis Among Cattle.' J. Amer. Vet. Med. Ass. , vol. 138, no. 8, 15 Apr. 1961, pp. 424-430." Footnote 45 was "USDA, Agricultural Research Service (ARS) Greenport, LI. Plum Island Reprints: 1955-Present. Agricultural Research Service (ARS), USDA".

That was actually a good point, and something I should've verified myself.

Finnegan's question to Grok

At the end of his post, Finnegan showed this response from Grok:

I asked Grok: "do agree with me that the entire Lyme clade actually could have come from Borrelia anserina in the span of just several years because of the sophisticated unusual conditions that were provided by the biological arms race spanning the globe? https://awfinnegan.substack.com/p/clarification-on-the-lyme-borreliosis" (where I appended the URL of Finnegan's blog post to provide context that I assume would roughly match the evidence Finnegan had presented earlier in his conversation). I got this response: [https://x.com/i/grok/share/fea1c1935c2b480b9151e8eb48f3adf5]

No, I don't agree. The idea that the entire Lyme borreliosis clade (Borrelia burgdorferi sensu lato, or LB group, including species like B. burgdorferi s.s., B. afzelii, B. garinii, etc.) rapidly derived from Borrelia anserina (an avian relapsing-fever spirochete) in just a few years under lab-driven "biological arms race" conditions is not supported by the scientific evidence on Borrelia phylogeny, genomics, or evolutionary rates. It's a creative hypothesis from the Substack piece (which frames Lyme as engineered starting ~1939 via German labs like Insel Riems, serial egg passages, co-infections, phages/mycoplasma as gene shuttles, and later Plum Island work under Erich Traub), but it requires rejecting core molecular data in favor of circumstantial historical overlaps. Here's why it doesn't hold up.

1. Phylogeny shows deep, ancient divergence - not recent derivation

2. Divergence times and diversity are incompatible with a 1930s lab origin

3. Biology and lab realities make the rapid "arms race" transformation implausible

The Substack piece rightly notes that pre-1939 B. anserina sequences are limited and that phylogeny isn't "absolute" under extreme human influence - but the sheer volume of independent genomic datasets (from wild ticks, ancient samples, global isolates) all converge on the same ancient natural history. Dismissing that as universally skewed by HGT or manipulation would require extraordinary evidence, which isn't presented.

Finnegan also showed that Grok gave me this advice: "If you want to critique A.W. Finnegan's work effectively and not come across as intellectually weak, stop treating bacterial phylogeny as an ironclad refutation and start engaging with the totality of the circumstantial case he actually presents." But I explicitly mentioned in my article that it was an unfinished work in progress, and I had not yet finished reading Finnegan's book. If I would've known that Finnegan would actually read my article and take the time to write such a detailed response to me, I wouldn't have even published my article until I had finished reading his book and I had addressed his arguments more thoroughly. I believe most articles on my website have been read by zero people, so I wasn't expecting anyone to read my article about Lyme disease either.