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

First published 2026-03-29 UTC, last modified 2026-04-17 UTC

This part is about Adam Finnegan and Erich Traub, but part 1 covers other topics: lyme.html.

Contents

The Sleeper Agent and Erich Traub

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 several 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".

When I googled for the name Dan Benjamin, the first person listed was a podcaster, but the second person was a diplomat born in 1961, who is the President of the American Academy in Berlin, who was previously a "Coordinator for Counterterrorism" at the US Department of State, and who earlier served as 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 diplomat Dan Benjamin 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.

(I think the tone of some of Grok's statements is too definitive, because for example Grok cannot know that Maclean had absolutely no involvement in any aspect of biological warfare programs. And there might be some serious historian who found a single piece of evidence that Maclean dealt with biological topics in some capacity, but maybe the historian never published the evidence. Initially Grok also claimed that Maclean had no education in biology, but I pointed out that even if Maclean would've taken a single course in biology in high school, it would've amounted to some education in biology. But regardless, Maclean doesn't seem like a person who would be designing insect bombs.)


Annie Jacobsen wrote: "Traub was recruited into the Accelerated Paperclip program by Dr. Blome's handler, Charles McPherson, and arrived in America on April 4, 1949." [https://avalonlibrary.net/ebooks/Annie%20Jacobsen%20-%20Operation%20Paperclip.pdf] She didn't cite any source, but elsewhere she referred to Kurt Blome's RG 330 file as a source of information about McPherson. She said that McPherson was a "member of the Special Projects Team for Accelerated Paperclip" who "recruited Dr. Kurt Blome to work on biological weapons research".

I didn't find any reference to Charles McPherson in the books by Finnegan, Linda Hunt, or Tom Bower, and the only reference to him in Lab 257 was a memorandum from McPherson that was cited in the bibliography. Finnegan wrote that Maclean was "Traub's handler" who "helped him get cleared for Operation Paperclip". But I didn't find any connection between Maclean and McPherson.

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 produced the following list of 6 points: [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] The full paper about the lecture is behind a paywall, but there's no reference to ticks in the part of the paper that is visible from the free preview, 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.

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 did actually move 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 was building 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 special operations pilot in the US Air Force, 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 if he is just a useful idiot who is being fed disinformation by Loftus. So therefore I have been trying to map out his network 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 Kurt Blome's RG 330 dossier 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 had been classified before the 80s.

In 2013 when someone did a FOIA request for files about Blome including the RG 330 file, 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.

Now of course it's possible that Traub's trip to Turkey is real, but I would like to see more evidence for the trip apart from a secret intelligence file that was supposedly uncovered by someone who worked for CNN. Or I would at least like to see the file itself instead of having to rely on descriptions about the file by people who are peddling false information about Nazis, like Linda Hunt, Tom Bower, and Adam Finnegan.


Later in his book Finnegan wrote: "Traub would take another mission for the FAO to Turkey to assist them in the setup of an FMD lab there, which took him from 1969 to 1972." And he cited this document: "Traub, E., et al. Turkey: Vaccine Production. FAO Report Number: AGA-DP/TUR/69/533, Accession Number: 120100. (1972)." So if Traub later took another trip to Turkey that is documented outside of secret intelligence documents, then I guess it increases the likelihood that Traub would've also taken an earlier trip to Turkey.

The story of Traub's first trip has a somewhat anticlimactic ending, which also makes the story more believable, because mundane and boring stories tend to be more believable than sensationalistic stories. A book which cited Blome's interrogation by ALSOS said: "Blome did not know any of the details as to how or where Traub actually obtained the virus. Traub returned to Reims with the virus and there, in an old building isolated from the main institute, an attempt was made to infect some cattle by rubbing the virus on their nose and mouth. One animal was sick, but recovered and the others were unaffected. Further work was therefore impossible as the strain had proved avirulent. On reporting this to Himmler at a later meeting, Blome was told that attempts would be made to secure another strain but he heard no more concerning the matter." [https://books.google.com/books?id=EjNlDwAAQBAJ&pg=PA170]


In a book chapter titled "Conversion of BTW Facilities: Lessons from German History", Erhard Geissler wrote: "In the final stage of WWII the institute was requested to develop a rinderpest vaccine because of German concern that her enemies might use rinderpest virus for BW attacks. There are contradictory reports whether at least small-scale experiments with Rinderpest virus had been performed at Riems by Waldmann's deputy Erich Traub and his coworkers." [https://annas-archive.gl/search?q=Conversion+of+BTW+Facilities+geissler] But he didn't specify why the reports were contradictory.

Traub's research on bacteria

Traub was a virologist, and he did not do much work with bacteria judging from his bibliography. Claims that he researched Borrelia bacteria go back to sources like unpublished intelligence files, or to anecdotal information conveyed by Loftus and Carroll, or to speculation based on his coworkers studying Borrelia.

Even on Finnegan's extensive timeline about Traub, there are only a few entries about Traub working with bacteria: [https://www.thesleeperagent.com/erich-traub]

Finnegan didn't list any study where Traub would have modified bacteria through methods like serial passage, or where Traub would have somehow weaponized bacteria (apart from the alleged modification of Serratia marcescens through use as a viral filter, which seems like some kind of a misunderstanding or misinterpretation by Finnegan).

So basically Traub was a virologist and not a bacteriologist, and he primarily worked on animal diseases and not human diseases, and he worked in the DC area and Colombia but not Plum Island, and he had likely moved back to Germany before people from USDA started to work at Plum Island. His main qualification for becoming the creator of Lyme disease seems to have been that he was a Paperclip Nazi, and John Loftus had earlier said that anynymous spies had speculated that Paperclip Nazis were responsible for Lyme disease.

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 the common reference strain 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 strain of B. burgdorferi had only about 96-97% identity to B. anserina:

# exclude plasmids, shotgun sequences, and intergenic spacers, remove 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 to Germany before the Plum Island lab opened

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 referred to a book about a symposium held at Plum Island in September 1956. [https://archive.org/details/CAT31325716/page/40] The book he cited 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 symposium. The opening day ceremony refers to the formal opening of both 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 January 1953, but I don't know if he had already moved to Germany by the time USDA scientists moved to Building 257 in 1953, or if people from USDA already worked in some limited capacity at Plum Island in 1952.

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.

Later in the book Finnegan wrote: "Dr. Galloway had been involved in the setup of the Colombian FMD lab in Bogotá for the FAO, maintaining it until Traub took it over from March 1951 to December 1952." Where he cited this document that I didn't find online: "Traub, E., & W.l. Capps. Report to the Government of Colombia on the Experiments with chick embryo-adapted foot-and-mouth disease virus. FAO Report Number: AN-EPTA 178 TA/272/S/2/, Accession Number: 050178. (1953)". So in October 1952 when the decision was made for Traub to move back to Germany, was he still in Colombia, and he didn't move back to the US until December 1952? Or was he in the US in October but he later visited Colombia again and returned back in December? Or was Traub somehow responsible for overseeing the lab up to December remotely, even though he had already returned to the US?

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 12th 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 in 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 did in reality travel to the US to attend a virology conference in 1958. The book about the conference is available at Anna's Archive, and it describes conversation between Traub and other people who took part in a symposium at the conference. [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 ever visited Plum Island.

Unnamed Nazi scientists at Plum Island

I haven't found any source published before Lab 257 where Erich Traub was named in connection to Plum Island. Grok also said: "No pre-2004 published sources (books, news articles, academic papers, or reports) have been identified that mention Erich Traub by name in direct connection with Plum Island." Carroll and Finnegan cite pre-2004 intelligence files where Traub was supposedly linked to Plum Island, but as far as I know, none of the files have been posted online, apart from a part of Standard Form 86 posted by Finnegan. And some of the files may have been fabricated to support the narrative about Traub.

Linda Hunt mentioned Traub in Secret Agenda but she didn't connect him to Plum Island, and she only mentioned that he worked for the Navy but not USDA. In the preface to The Belarus Secret, John Loftus did not mention Traub but only unnamed Nazi scientists at Plum Island.

A Scientific American article from 2000 also mentioned unnamed plural Nazi scientists but not Traub: [https://resourcespacec2.svsu.edu/mount/library/archives/public/Follett/documents/144_151/KFP148_81d.pdf]

"We still get asked about the Nazi scientists," says Sandy Miller Hays, the slightest trace of weariness creeping into her voice. We're sitting on the ferry that will bring us back from Plum Island, where the U.S. Department of Agriculture (USDA) operates one of the world's top laboratories for the study of infectious animal diseases.

Foot-and-mouth disease and African swine fever would not seem to be the stuff of wild urban legend anymore. Nevertheless, the rich mythology that has sprung up around the 840-acre island makes it a must-see stop on the conspiracy theorist's world tour. Hays, information director for the department's Agricultural Research Service, which oversees the laboratory, patiently describes several of the choice tales she's been asked about over the years. The gist of the "Nazi scientists" story is that after the war the army (which did actually use Plum Island as a base to hunt U-boats) brought German scientists to the island to develop biological-warfare agents. Lyme disease, first identified in nearby Connecticut, was caused by one of their escaped microbes, according to the tale. Other stories feature three-headed mutant chickens, space aliens in storage and a secret submarine laboratory.

A Newsweek article from 2001 also referred to unnamed plural Nazi scientists: "One local story has it that eight-foot chickens have free run of Plum Island. Or Nazi scientists were taken there to develop Lyme disease, which they shot from a cannon across the sound to the woods of Connecticut. 'My personal favorite is the one that we actually shot down a UFO and are holding the aliens for study,' says Thomas Sawicki, the chief safety officer, who despite his sense of humor still refuses to allow visitors access to some areas of the lab." [https://www.newsweek.com/foot-and-mouth-wars-150247]

Steve Nostrum and Karl Grossman became involved in Lyme activism in the 1990s, but I didn't find evidence that they mentioned Traub anywhere before 2004.

Finnegan responds to me at Substack

In March 2026 Finnegan posted a 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.

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 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 uniformly but the mutations would be concentrated in the parts of the genome that are targeted by the antibiotics. Many species of bacteria have developed antibiotic resistance in the past century, 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 recently 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.

Finnegan also wrote: "When comparing Borrelia burgdorferi to Borrelia anserina as a whole, that is, the morphological characteristics, genetic similarities, and host compatibility, the two are in fact extremely similar. Morphologically speaking - in size, shape, and ultrastructure - They both exhibit comparable lengths (roughly 8-21 μm), wavelengths (1.7-3.0 μm), diameters (0.22-0.38 μm), pointed ends, and flagellar arrangements (typically 7-11 sheathed flagella with similar surface-layer architecture).[60]" But it's expected for related species to have similar morphology, and it's not evidence that one species was engineered from the other. Chimps have similar height and shape as humans, and the same number of arms and legs, so does that mean that humans were created from chimps by Nazis?

Anserina as an outgroup in a rooted tree

Finnegan wrote: "Richard Marconi had in fact put forward in his paper that the Lyme Borreliosis clade descended from Borrelia anserina, which served as an outgroup". In the paper by Marconi et al., the authors made a phylogenetic tree where they picked anserina as the outgroup, but that doesn't mean the authors suggested the other species were descended from anserina: [https://journals.asm.org/doi/pdf/10.1128/jcm.33.9.2427-2434.1995]

(The double slash symbol in the branch for anserina means that the true length of the branch is not displayed, because the branch would've taken about three times as much space as the whole width of the figure.)

If you want to turn an unrooted tree to a rooted tree, you have to pick some node as an outgroup. Then the earliest branch in the tree will be formed between the outgroup and other nodes. It's typical for the node that is the most distant from the main cluster of nodes to be selected as the outgroup, like how in Marconi's tree there were 11 nodes from the LB group and 1 node from the RF group, so the node from the RF group was selected as the outgroup. If the authors would've made a tree with 11 nodes from the RF group and one node from the LB group, the authors could've similarly selected the node from the LB group as the outgroup, but that doesn't mean that the authors would've suggested that the RF group was descended from the LB group.

If you don't know how to interpret an unrooted tree, and you don't know that the deepest split is undefined in an unrooted tree, then from the unrooted tree below, it might appear like the deepest split is between andersonii and the other species, even though in reality the branches are unordered in an unrooted tree. But in the rooted tree where anserina is the outgroup, the deepest split is now defined, and the first branch in the tree is intuitively between anserina and the other nodes:

# 16S sequences of 9 strains from Marconi's paper and substitutes for 3 strains I didn't find at GenBank
echo 'L46688.1,andersonii 19857
L46701.1,andersonii 21038
L46695.1,japonica IKA2
L46696.1,japonica HO14
L46697.1,afzelii J1
NR_104748.1,afzelii VS461
M84815.1,afzelii IP3
U42284.1,anserina ES-1
AF467957.1,burgdorferi B31
NR_043413.1,garinii 20047
AJ009753.1,garinii Far04
AF467970.1,americana SCW-41'>accessions

# download and align sequences
curl 'https://eutils.ncbi.nlm.nih.gov/entrez/eutils/efetch.fcgi?db=nuccore&rettype=fasta&id='$(cut -d, -f1 accessions|tr \\n ,)|mafft ->marconi.fa

# omit parts from start and end of alignment where some sequences have gaps
seqkit subseq -r 30:1292 marconi.fa>marconi2.fa

# make an unrooted ML tree
iqtree3 -nt AUTO -s marconi2.fa
library(ggtree)

t=read.tree("marconi2.fa.treefile")
t$tip.label=fread("accessions",head=F)[,V2[match(t$tip.label,V1)]]

# t=ape::root(t,"anserina ES-1",resolve.root=T) # uncomment for rooted tree

ggtree(t)+geom_tiplab()+
hexpand(ratio=.2,direction=1)+
ggtitle("Unrooted")+
theme(plot.title=element_text(hjust=.5,face=2,size=12))
ggsave("1.png",height=length(t$tip.label)*.17,width=5)

Kanhai's studies in serial passage and cell fusion

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 Traub and his coauthors actually wrote 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]

So 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 FMD virus so eventually it was not able to sustain another passage, which he compared to the natural ending of a disease outbreak in animals.

Similarly Traub didn't claim he had altered the FMD virus to give it the property of "reduced suspectibility in undernourished individuals". But he pointed out that in the same way that undernourished cows appeared to be less suspectible to FMD than well-nourished cows, a cell line that was given a nutrient-poor growth medium was less susceptible to infection than a cell line that was given a nutrient-rich growth medium.

Next Finnegan showed the screenshot of the study below and wrote: "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."

The study did not result in T. parva becoming adapted to hamsters. [https://www.sciencedirect.com/science/article/abs/pii/0020751974900708] 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.

Amount of genetic change caused by adaptation to a new host

Finnegan wrote: "When Erich Traub had Werner Schäfer acquire and maintain Borrelia anserina from Franz Jahnel in serial egg passages for his institute starting in 1939, several attempts had already been made previously trying to adapt Borrelia anserina to a variety of new hosts like mice and other animals, change its tropisms to be more neurotropic in order to serve as a comparable animal model for the study of syphilis. This was noted by Franz Jahnel in a section of a 1936 book titled 25 Years of the Kaiser Wilhelm Society for the Advancement of the Sciences (25 Jahre Kaiser Wilhelm-Gesellschaft ƶur Förderung der Wissenschaften), in a section titled Institute for Spirochetal Research (Institüt für Spirochätenforschung). He cites numerous attempts to adapt the avian spirochete to mice, lizards, turtles, frogs, fish, and pigeons by other researchers.[12] This shows the desire to adapt it to new hosts and remodel it altogether was already in growing demand before WWII."

I pasted Finnegan's text to Grok and wrote: "How many percent would modification like this cause the chromosome of Borrelia anserina to change? Paragraphs-only answer in about 300 words. When referring to a specific source or study, put the URL of the source in square brackets after a sentence." I got this response:

The chromosome of Borrelia anserina undergoes extremely limited sequence alteration from laboratory modifications such as serial egg passages and experimental attempts to adapt the spirochete to novel hosts like mice, lizards, turtles, frogs, fish, or pigeons. These procedures, as pursued in the 1930s by researchers including Franz Jahnel and later maintained through egg passages under Erich Traub and Werner Schäfer, rely on selective pressure in vivo or in ovo to favor variants better suited to new environments or to shift tissue tropisms. However, the linear chromosome of approximately 905 kilobases encodes essential housekeeping genes with high synteny across isolates, rendering it resistant to wholesale remodeling. Instead, adaptation typically involves minor point mutations, small indels, or plasmid-level variations that fine-tune surface proteins or virulence without disrupting core genomic architecture. Whole-genome comparisons of sequenced B. anserina strains confirm this stability, showing that even strains maintained under differing laboratory conditions diverge by only a handful of nucleotide positions. [https://pmc.ncbi.nlm.nih.gov/articles/PMC5356049/]

Alignment of the chromosome from strain Es (906,833 base pairs) with strain BA2 (904,790 base pairs) identifies just four transversions and 37 single-nucleotide indels across the shared sequence. This results in roughly 0.005 percent overall divergence, a level so low that it represents negligible change for practical purposes. Comparable conservation appears across Borrelia species, where chromosomal gene content and order remain nearly identical despite ecological specialization, underscoring that host-switching experiments do not drive rapid or extensive chromosomal evolution. In related attenuation studies using serial passages in liquid medium rather than eggs, loss of chick infectivity by the twelfth passage correlated with shifts in protein profiles detectable by electrophoresis, yet electron microscopy revealed no structural genomic differences and no evidence of broad chromosomal mutation. [https://pubmed.ncbi.nlm.nih.gov/2300719/]

These findings indicate that the pre-World War II efforts to remodel Borrelia anserina for neurotropic or mammalian models produced at most trace chromosomal tweaks through natural selection during limited passages, far below thresholds that would redefine the organism's genetic identity. Plasmids, which carry many variable surface antigens, absorb most adaptive burden, leaving the chromosome essentially intact at greater than 99.99 percent identity to progenitor strains. Consequently, modifications of the type described would alter the B. anserina chromosome by approximately 0.005 percent, preserving its fundamental sequence and synteny while permitting phenotypic shifts sufficient for experimental utility. This genomic resilience explains why avian spirochetosis agents have retained their core identity despite decades of laboratory manipulation.

Then I asked: "Does adaptation of bacteria to a new host species through serial passage increase the rate of substitutions per site per year in the chromosome by several orders of magnitude compared to natural conditions? (~200 words)" I got this response:

Yes, substitutions per site per year can increase by several orders of magnitude during serial passage or experimental adaptation to a new host compared with long-term natural evolutionary rates. Bacterial long-term molecular clock estimates, calibrated over geological or ecological timescales in wild populations, typically range from 10^{-10} to 10^{-9} substitutions per site per year because purifying selection removes most mutations over time. In contrast, short-term rates measured during within-host evolution, host shifts, or laboratory serial passage routinely reach 10^{-7} to 10^{-5} substitutions per site per year - a 100- to 10,000-fold acceleration. This discrepancy arises because serial passage compresses hundreds of generations into calendar weeks or months, imposes intense directional selection for host adaptation or faster replication, and creates repeated population bottlenecks that enhance genetic drift and rapid fixation of beneficial (or even slightly deleterious) variants before purifying selection can act. [https://pmc.ncbi.nlm.nih.gov/articles/PMC5053366/]

For spirochetes like Borrelia anserina, the same pattern applies: laboratory egg passages or attempts to shift tropism fix chromosomal changes far faster than in natural avian-tick cycles, where replication is slower and selection weaker. Experimental evolution studies in other bacteria (e.g., Mycoplasma after host jumps or Pseudomonas during in vivo passage) confirm substitution accumulation rates up to ~10^{-5} per site per year over just a few years, orders of magnitude above natural baselines. These elevated short-term rates do not reflect a change in the intrinsic mutation rate per replication but rather the accelerated observable evolution under artificial conditions. Once returned to natural-like environments, the molecular clock slows dramatically as deleterious mutations are purged. Thus, serial passage genuinely inflates substitutions per site per year by several orders relative to steady-state natural conditions.

But even 1e-5 substitutions per site per year would still amount to only about 0.01% divergence away from the source strain after 10 years, and nowhere near the 25% divergence between anserina and burgdorferi.

And adaptation to a new host species would primarily result in the selection of nonsynonymous mutations in protein-coding sequences, but anserina and burgdorferi are also divergent in non-coding regions, and they also differ by a huge number of synonymous mutations.

From the plot below where I compared the flagellin genes of anserina and burgdorferi, you can see that there's about 4 times as many synonymous mutations as nonsynonymous mutations, which indicates that the gene is under negative selection pressure:

curl 'https://eutils.ncbi.nlm.nih.gov/entrez/eutils/efetch.fcgi?db=nuccore&rettype=fasta&id=NZ_CP161191'|seqkit subseq -r147678:148688|seqkit seq -rp>flabb.fa
curl 'https://eutils.ncbi.nlm.nih.gov/entrez/eutils/efetch.fcgi?db=nuccore&rettype=fasta&id=NZ_CP005829'|seqkit subseq -r146345:147349|seqkit seq -rp>flaba.fa

# codon align
coda()(x=$(cat);seqkit seq -g <<<"$x"|seqkit translate|mafft --quiet -|seqkit seq -s|awk -F '' 'NR==FNR{gaps=0;for(i=1;i<=NF;i++)if($i=="-")a[NR][i-(gaps++)]++;next}{for(i=1;i<=NF;i+=3){i2=(i-1)/3+1;for(j=1;j<=a[FNR][i2];j++)printf"---";printf"%s",substr($0,i,3)};print""}' - <(seqkit seq -gs<<<"$x")|paste <(seqkit seq -n<<<"$x") -|seqkit tab2fx)

# run SNAP.pl for a pair of sequences
sna3()(sna "$@";(echo position,synonymous,nonsynonymous,indel;awk '/^[0-9]/{print$1,$7?$7:0,$8?$8:0,$2=="indel"}' OFS=, $(ls -t codons.*|head -n1))>snap.csv)

# install SNAP.pl
mkdir -p ~/bin;curl https://www.hiv.lanl.gov/repository/aids-db/PROGS/Snap/SNAP.pl>~/bin/snap;chmod +x ~/bin/snap

cat flab[ab].fa|coda|sna3
t=fread("snap.csv")
p=setNames(melt(t,id=1),c("x","z","y"))[,y:=cumsum(y),z]

ybreak=pretty(p$y,7);xbreak=pretty(p$x,7)+1
xmin=1;xmax=max(p$x);ymin=0;ymax=max(ybreak)

ggplot(p)+
geom_rect(color="gray75",xmin=xmin,xmax=xmax,ymin=ymin,ymax=ymax,linewidth=.4,fill=NA,lineend="square",linejoin="mitre")+
geom_step(aes(x,y,color=z),linewidth=.6)+
labs(title="Cumulative mutations in flagellin gene (anserina vs burgdorferi)",x=NULL,y=NULL)+
scale_x_continuous(limits=c(xmin,xmax),breaks=xbreak)+
scale_y_continuous(limits=c(ymin,ymax),breaks=ybreak)+
scale_color_manual(values=c("#00cc00","red","blue"))+
coord_cartesian(clip="off",expand=F)+
theme(axis.text=element_text(size=11,color="gray40"),
  axis.text.x=element_text(margin=margin(3)),
  axis.text.y=element_text(margin=margin(,3)),
  axis.ticks.length=unit(0,"pt"),
  legend.background=element_blank(),
  legend.box.spacing=unit(0,"pt"),
  legend.margin=margin(,,4),
  legend.justification="right",
  legend.key=element_blank(),
  legend.key.height=unit(13,"pt"),
  legend.key.spacing.x=unit(2,"pt"),
  legend.position="top",
  legend.spacing.y=unit(0,"pt"),
  legend.text=element_text(size=11,vjust=.5,margin=margin(,,,2)),
  legend.title=element_blank(),
  panel.background=element_blank(),
  panel.grid.major=element_line(linewidth=.3,color="gray85"),
  plot.subtitle=element_text(hjust=.5,margin=margin(,,3)),
  plot.title=element_text(size=11,hjust=.5,margin=margin(,,3)))
ggsave("1.png",width=4.8,height=3.2,dpi=300*4)
system("magick 1.png -resize 25% -dither none -colors 256 1.png")

In one study sheep were infected with a human-adapted strain of Staphylococcus aureus, which is able to infect sheep but results in milder illness in sheep than sheep-adapted strains of Staphylococcus aureus. [https://www.science.org/doi/10.1126/sciadv.aax0063] Infection chains of up to 8 sheep were achieved by infecting subsequent sheep with bacteria obtained from the milk of previously infected sheep. After 400 days of passage between sheep, there were only about 8 mutations on average per sample. The genome of Staphylococcus aureus is about 2.8 megabases long, so 8 mutations per 400 days corresponds to about 3e-6 substitutions per site per year (from 8/400*365/2.8e6). At that rate of mutation, it would take about 100,000 years of passage through sheep for the genome to change by 25%, even though 3e-6 substitutions per site per year is a very fast rate of mutation, and the rate of mutation would eventually slow down as the bacteria would become adapted to the new host species (and it might not even be possible to sustain passage indefinitely).

In the sheep study, nonsynonymous mutations were about 3 times as common as synonymous mutations, which indicates that there was high selection pressure during adaptation to a new host species. But my plot above shows the opposite pattern, which indicates that the genetic divergence between anserina and burgdorferi is not because of some kind of hyper-accelerated evolution that occurred over the course of a few years.

HGT cannot explain 25% divergence throughout the chromosome

I'm sorry for relying on LLMs again, but ChatGPT gave me the following explanation for why horizontal gene transfer cannot explain the divergence between anserina and burgdorferi:

Finnegan's use of horizontal gene transfer (HGT) rests on a fundamental mischaracterization of what HGT can and cannot do at the genomic level. In bacteria, HGT is indeed a real and important evolutionary mechanism, but it operates in a modular and localized manner, not as a whole-genome rewriting process. Typical HGT events involve the acquisition of discrete genetic elements - plasmids, transposons, pathogenicity islands, or occasionally individual genes - often conferring specific traits such as antibiotic resistance or metabolic capabilities. These transferred elements integrate into an otherwise intact genomic backbone that retains the organism's evolutionary history. As a result, while HGT can create mosaic genomes, it does not erase the underlying phylogenetic signal distributed across hundreds to thousands of conserved genes.

The key error is the leap from "genes can move between organisms" to "entire species-level divergence patterns can be artificially generated in a short time." Species within the Lyme borreliosis group differ not by a handful of horizontally acquired loci but by genome-wide sequence divergence, including synonymous substitutions, regulatory differences, gene content variation, and conserved housekeeping genes that are not freely exchanged. To recreate that level of divergence artificially via HGT would require coordinated replacement or transformation of a substantial fraction of the genome across multiple independent lineages. There is no known biological mechanism - natural or engineered, especially in the mid-20th century - that can accomplish this at scale. Even modern synthetic biology cannot rewrite bacterial genomes across populations in the way this claim requires without leaving clear, detectable signatures.

Additionally, HGT is constrained by multiple biological barriers that Finnegan does not account for. Successful gene transfer depends on compatibility between donor and recipient systems, including promoter recognition, codon usage, protein folding environments, and regulatory integration. Many transferred genes are neutral or deleterious and are purged by selection. Even when beneficial, they typically remain identifiable as foreign insertions due to differences in GC content, phylogenetic incongruence, or flanking mobile elements. In contrast, the divergence observed among Lyme Borrelia species is internally consistent across the genome, not patchy or anomalous in the way extensive HGT-driven remodeling would produce.

Another critical point is that phylogenetic reconstruction does not rely on single genes that could be horizontally transferred, but on concordance across many independent loci. Even in organisms with known HGT, researchers can detect and exclude transferred genes or use core-genome approaches to recover the vertical inheritance signal. For Finnegan's scenario to hold, HGT would need to systematically overwrite or obscure this signal across the majority of the genome in multiple species simultaneously, while still producing a coherent tree-like structure that matches observed data. This is not just unlikely; it is incompatible with how recombination and gene transfer actually behave in bacterial populations.

Finally, empirical observations directly contradict the proposed magnitude of HGT effects. In well-studied systems where HGT is rampant - such as antibiotic resistance spread in hospital pathogens - the result is not the rapid emergence of entirely new species, but rather strain-level variation within existing species frameworks. The core genome remains stable enough that phylogenetic relationships are still recoverable and consistent with evolutionary timescales. Finnegan's argument effectively treats HGT as a mechanism capable of compressing millions of years of divergence into a few years, but there is no experimental, genomic, or theoretical support for such a capability.

Did Traub work at Plum Island from the beginning?

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."

It's not clear if Finnegan meant from the beginning of Traub's stay in the US in 1949-1953, or from the beginning of when USDA scientists started to work at Plum Island in 1953 or 1952, even though he wrote that Traub "was back and forth between Colombia in South America and Plum Island, NY, from 1949-1952,[30] loosely in parallel with the bird migration patterns" (where he cited Traub's JIOA file). And in his book Finnegan wrote that Traub had already supervised "simulant tests around Plum Island" in late 1951.

Finnegan also posted the image below and 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]"

When I googled for the term "Greenport Long Island Station" in double quotes, all matches for the exact term came from Finnegan. However even the image above doesn't feature the exact term, but in the image Traub's "duty station" is listed as "Greenport, L. I., New York". And in his book Finnegan wrote the term in the form "Greenport, Long Island station", where the word "station" was not capitalized. So I think Finnegan came up with term "Greenport Long Island Station" based on the form where Greenport was listed as the duty station, and the word "station" should not be capitalized in the term, because it gives the impression that "Greenport Long Island Station" is some kind of a fixed term that acts as a proper noun.

But anyway, Finnegan wrote in his book that "on January 14, 1953, Traub and his family boarded the SS Stockholm, and sailed back to Germany", and that Traub even visited Switzerland in the spring of 1953. But a history of ARS says that the name Agricultural Research Service was only adopted in November 1953: "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 Traub would have worked for the Agricultural Research Administration before it had been renamed to Agricultural Research Service, but he or whoever filled the form later used the new name to refer to Agricultural Research Administration.

However in his book Finnegan specifically wrote that Traub 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)." 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]

In his blog post 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 even specify that a research center should be created at Plum Island, and the process of selecting the location for 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, the renovations for 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 [by Carroll]]

[...]

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 hearings took place in July 1952, which was only about half a year before Traub moved back to Germany.

The oldest newspaper article I found about a proposed laboratory on Plum Island was from February 26th 1952. The article said: "There has been substantial interest in establishment of a U.S. laboratory for research on hoof-and-mouth disease for some time, but little progress was made until the widespread outbreak of the disease in Mexico in 1946 and the subsequent outbreak early this year in Canada near the U.S border." [https://www.newspapers.com/article/lincoln-farm-and-home-news/194492237/] The Canadian FMD outbreak was officially confirmed on February 25th, when a quarantine was imposed on the area around the outbreak, even though a veterinarian suspected an outbreak of FMD on February 12th, and he sent samples for testing on February 16th. [https://www.producer.com/livestock/the-road-to-foot-and-mouth-was-long-but-the-path-was-short/]

A large number of newspaper articles about the proposed laboratory began 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 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. The news followed hard on the heels of a Department of Agriculture proposal to set up a lab for the stud of hoof and mouth discase on the islet." [https://www.newspapers.com/article/newsday-nassau-edition/194427451/] At the time, even the laboratory by the Chemical Corps was still said to be only a proposed laboratory. The article quoted a representative from USDA as saying that "the proposed Army laboratory has no bearing on the Department of Agriculture's decision to study hoof and mouth disease" (which might have been a lie). The article also said: "Long Island and state legislators and officials are girding for battle to prevent Plum Island from being used by the Department of Agriculture for a hoof-and-mouth discase lab or by the Army for a research project in germ warfare. The cattle disease project could be halted by existing bills, but there is no such protection for Long Island against the Army's research."

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." The hearings required by the amendment were conducted later the same month. Perhaps the backup plan was to set up the lab under the auspices of the Chemical Corps in case the USDA did not receive a permission to build the lab.

Standard Form 86

I found a scan of a filled form using the same Standard Form 86 template as Traub's supposed form: [https://archive.org/details/RichardCharlesHolbrooke/page/n351/mode/2up]

Here's Traub's supposed form again for comparison:

Standard Form 86 was titled "Security Investigation Data for Sensitive Position", which doesn't seem like the type of form that would be required for traveling to the US to attend a virology conference, but rather for applying for a new job position.

Grok said:

The document you shared (and the similar one in the previous image) is an internal federal agency transmittal or cover sheet used in the 1950s when processing personnel appointments or pre-appointment security investigations. Key indicators:

This was not a general visa application, entry form, or symposium registration document. It was part of the civil service / federal hiring pipeline, especially for excepted-service scientific roles like the "Chief Scientist (Virology and Bacteriology)" position on the Greenport/Plum Island form.

The form said: "If this is a request for investigation before appointment, insert 'APPL' in the space for Date of Appointment and show information about the proposed appointment in the other spaces for appointment data." In Traub's form the date field was empty, so it wasn't clear if the form referred to his past or current or future employment, even though under "type of appointment" in the form, the box "expected" was checked, which gives the impression that the form referred to future employment. So in case the form is actually real, one possibile scenario might be that Traub briefly did some work at Plum Island while he visited the US in 1958, so he needed to fill the form because of it. But then again it would be weird that his job title would've been "Chief Scientist (Virology and Bacteriology)", and for some brief work he did while he visited the US, he wouldn't have necessarily even been appointed as an employee at USDA, unless an employment position was somehow required for a security clearance. So I would like to see the full form, or preferably the full FBI file the form was part of.

B. T. Simms

Finnegan wrote: "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)."

Simms was the head of the USDA's Bureau of Animal Industry, which was placed under the Agricultural Research Administration in 1942, and in 1953 Agricultural Research Administration was renamed to Agricultural Research Service. [https://mag.auburnvetmed.com/remembering-b-t-sims/] Simms later briefly served as the director of Plum Island. However the Plum Island laboratory did not yet exist in 1950 when Simms was listed as Traub's point of contact, and just because Simms later worked at Plum Island, it doesn't mean that Traub himself worked at Plum Island.

Meaning of supervisory bacteriologist

Finnegan wrote: "Traub was listed as a supervisory bacteriologist in his intelligence file, so he was clearly overseeing simulant tests". In his book Finnegan wrote: "These factors were relevant and form part of the reason Traub was chosen as, among other duties, a 'supervisory bacteriologist' for the American military, to supervise bacterial simulant tests, listed in the JIOA (Joint Intelligence Objectives Agency) file on Erich Traub.[26]"

When I googled for the term "supervisory bacteriologist" in double quotes, there were only 2 pages of results. There were only 4 results that were not about Traub, which were all old documents from 1930-1959, but they didn't explain what the term "supervisory bacteriologist" meant.

However I found an article at Newspapers.com that said: "Following service in the Army Air Corps, Mr. Dashiell went to Fort Detrick as a bacteriologist in 1951. Since then he has been promoted to supervisory bacteriologist, supervisory chemical engineer, staff chemical engineer and finally to project engineer before being assigned, in 1969, as the assistant scientific director for development and engineering". [https://www.newspapers.com/article/the-daily-times/194500387/] So is a supervisory chemical engineer also someone who supervises chemtrail experiments? I think a supervisory bacteriologist just means something like a senior bacteriologist, or a bacteriologist in a supervisory role.

I also found a job listing for the title of "Supervisory Bacteriologist" from 1965, which said that "A young male graduate bacteriologist experienced in sterilization techniques is required for a responsible production supervisory position in a well known Montreal pharmaceutical plant." [https://www.newspapers.com/article/the-montreal-star/194500366/]

Mike Carroll's anonymous source

Finnegan wrote:

Michael C. Carroll, author of Lab 257: The Disturbing Story of the Government's Secret Plum Island Germ Laboratory shows that Plum Island sources had discussed seeing pictures of Traub pointing to the sections of the island where he had released ticks for insect simulant tests:

A source who worked on Plum Island in the 1950s recalls that animal handlers and a scientist released ticks outdoors on the island. "They called him the Nazi scientist, when they came in, in 1951 - they were inoculating these ticks," and a picture he once saw "shows the animal handler pointing to the area on Plum where they released the ticks."[29]

I would've written that Carroll "claims" instead of Carroll "shows", because he might have just made up the story.

Finnegan said that Carroll was talking about simulant tests, even though Carroll didn't specify if the tests were simulant tests or not. And in fact two pages earlier Carroll quoted John Loftus as writing that "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" and that "I explored the old spies' hypothesis that the poison ticks were the source of the Lyme disease spirochete". So Carroll gave the impression that his anonymous source was talking about the same event as Loftus.

Finnegan also claimed that the person in the picture was Traub, but the anonymous source said that the person in the picture was "the animal handler", who was probably not the same person as the Nazi scientist, because Carroll wrote that "animal handlers and a scientist released ticks", which seems to imply there was a single scientist and two or more animal handlers.

Apart from Carroll's anonymous source who might not even be a real person, I haven't found any person who worked at Plum Island or USDA saying that Traub visited Plum Island, or that Traub was seen on Plum Island. A New York Times article from 2004 included these commetns from the ARS spokeswoman Sandy Miller Hays: [https://web.archive.org/web/20150528042901/http://www.nytimes.com/2004/02/15/nyregion/heaping-more-dirt-on-plum-i.html?pagewanted=2]

She said she did not know of Erich Traub's connection, if any, to the island. "I have heard this Nazi scientist stuff for years and I never heard anything where anyone said 'that's right,'" she said.

Sandy Miller Hays didn't personally work on site at Plum Island, but she sometimes visited Plum Island, and she acted for a long time as the spokesperson of ARS on issues including Plum Island, so if Traub would've actually worked at Plum Island, she might have heard about him from current or former staff members of Plum Island. (Even though on the other hand USDA scientists may have started to work at Plum Island only after Traub had left the United States, so if Traub worked at Plum Island in some kind of a secret capacity before USDA moved in to Plum Island, then USDA staff might not have heard about Traub's work.)

It's also telling that Mike Carroll did extensive archival research about Plum Island, and he cited many pieces of correspondence from people who worked at USDA or Plum Island in the 1950s, and he interviewed many people connected to Plum Island, but he still wrote that the three confirmed occasions when Traub visited Plum Island all took place after Traub had already moved out of the United States.

Carroll himself doesn't seem to have treated the episode of ticks being released as a confirmed instance of Traub visiting Plum Island, because Carroll didn't include it on his list of three confirmed occasions when Traub could be physically placed on Plum Island.

It's not clear if the story is that the experiment of releasing the ticks in 1951 seeded the Lyme disease outbreak, or if the experiment was a simulant test like Finnegan says, or if it was an additional release of Lyme disease that followed an earlier release, or if it was some kind of a release of "poison ticks" that somehow delivered a chemical poison but that were not infected with any species of bacteria. In his book Finnegan wrote that Traub returned from Colombia to the US in early September 1951, "just in time to supervise simulant tests around Plum Island". But elsewhere Finnegan wrote that Donald Maclean may have already seeded the Lyme outbreak during his stay in the US in 1944-1948 when he "is said to have been directing Plum Island tests".

According to a history of Plum Island, the US Army Chemical Corps had been planning an animal research laboratory on Plum Island since 1951, but I don't know if it would've been before or after the ticks were supposedly released in 1951. [https://web.archive.org/web/20051103165628/https://usaha.org/news/newsletter/USAHA-Newsletter-Oct2003.pdf]

In the scenario where the release of ticks really took place, and the ticks were infected with Borrelia burgdorferi and not a simulant species, then what would be the point of releasing the ticks at a location where a biological research facility was planned to be built in the future? Wasn't there a worry that the staff of the facility might get sick in the future?

The earlier plan to build the laboratory on Prudence Island was killed by opposition by the local population, and the Plum Island plan was not popular either. So wasn't there a worry that the local population would be opposed to the lab if they found out that a dangerous new pathogen had been deliberately released near their home?

Now if the Soviets wanted to release a bioweapon in America and blame it on an American laboratory, it would make sense to release the bioweapon near an American bioweapons laboratory, in the same way that it would've made sense for Americans to release SARS-CoV-2 near the Wuhan Institute of Virology. And Finnegan does speculate that Traub was a Soviet agent. But I don't see what motive Americans themselves would've had to deliberately release Lyme disease near Plum Island.

Research of tick-borne pathogens in livestock at Plum Island

Finnegan 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".

The study on leptospirosis was in fact one case where people at Plum Island did research spirochetes, even though leptospirosis doesn't seem to have been a major focus of research for PIADC, because I didn't find any other paper about leptospirosis on a list of hundreds of papers coauthored by researchers at PIADC. [https://www.dhs.gov/sites/default/files/2024-06/24_0617_st_piadc_%20bibliography_1954-2024_0.pdf] Grok said:

No, I couldn't find any other studies on spirochetes (or spirochaetes) by researchers affiliated with the Plum Island Animal Disease Center (PIADC). Your assessment matches what the available evidence shows: the single leptospirosis paper you referenced appears to be the only instance of spirochete-related research in the entire official PIADC bibliography (1954-2024), and leptospirosis was never a major focus there.

I directly checked the DHS-provided bibliography PDF you linked (a comprehensive collection of hundreds of peer-reviewed papers coauthored by PIADC scientists). It contains no other titles mentioning Leptospira, leptospirosis, or any other spirochete genera/diseases (e.g., Borrelia, Treponema, Brachyspira, Spirochaeta, Lyme disease, swine dysentery, relapsing fever, etc.). Targeted searches of the full document for those keywords turned up nothing beyond the one leptospirosis case.

Broader literature searches (including PubMed-indexed results and general web queries for PIADC/Plum Island + spirochete/Borrelia/Leptospira/Treponema/Brachyspira publications or studies) also yielded zero additional scientific papers or research reports from PIADC personnel.

Finnegan claimed that Roger Breeze said that the Plum Island center "never worked with spirochetes or tick-borne disease", but actually Breeze only mentioned spirochetes but not tick-borne pathogens in general, because Verdon quoted him as writing: "In response to your questions, I can most definitely state that the USDA Agriculture Research Service does not conduct any research on spirochetes, including the agent of Lyme Disease and its anthropoid vectors, no research is planned, and none has been conducted since the Center was opened in 1953. Furthermore, no other government agency has conducted such experiments at Plum Island while this Center has been in existence." [https://books.google.com/books?id=EGa2KJjgBW0C&pg=PA13]

Heartwater (caused by Ehrlichia ruminantium) and East Coast fever (caused by Theileria parva) are both diseases that affect cattle and that are associated with major economic loss in countries where they are endemic. So research of heartwater and East Coast fever fits within Plum Island's mandate to study "foot-and-mouth disease and other animal diseases which in the opinion of the Secretary constitute a threat to the livestock industry of the United States". [https://www.law.cornell.edu/uscode/text/21/113a] Leptospirosis also affects humans, but the paper Finnegan referred to was about leptospirosis in cattle.

In his post Finnegan was wondering "why Plum Island didn't take any interest in Lyme disease and its co-infections when the outbreaks began happening right in their backyard - since those types of foreign animal diseases were exactly the kinds of diseases that Plum Island was set up to handle and put study into". But isn't Lyme disease primarily viewed as a domestic human disease and not a foreign animal disease?

Borrelia burgdorferi can infect horses, cattle, sheeps, goats, and pigs, but the infection is often considered asymptomatic or subclinical in livestock animals. The earliest paper I found about a Borrelia burgdorferi infection in livestock was published in 1988. [https://pubmed.ncbi.nlm.nih.gov/3190095/]

A paper from 2018 said: "Documented, naturally occurring syndromes attributed to B. burgdorferi infection in horses include neuroborreliosis, uveitis, and cutaneous pseudolymphoma. Although other clinical signs such as lameness and stiffness are reported in horses, these are often not well documented." [https://onlinelibrary.wiley.com/doi/full/10.1111/jvim.15042]

The economic loss associated with Lyme borreliosis in livestock seems to have received little attention. However a paper from 2022 said that symptoms of Lyme borreliosis in cattle may include decreased milk production and chronic weight loss. [https://pmc.ncbi.nlm.nih.gov/articles/PMC9146932/]

Another reason why Lyme disease was not studied at Plum Island might be if Borrelia burgdorferi was not recognized as a pathogen with potential to be employed as a bioweapon against livestock.

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 included the URL of Finnegan's blog post to provide context that I assume would roughly match the context 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 that 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. But 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.

Further topics

Did Fort Terry operate as a biological warfare testing site in the 40s?

The Wikipedia article about Erich Traub says: "Fort Terry on Plum Island was part of the U.S. biological warfare program in 1944-46, working on veterinary testing in connection with the weaponization of brucellosis." [https://en.wikipedia.org/wiki/Erich_Traub] But there's no source cited.

In his book Finnegan wrote that "Plum Island was conducting biological warfare tests in 1944 with brucellosis", and he cited a book chapter that said: "In November 1942, Secretary of War Stimson requested the Chemical Warfare Services (CWS) to prepare to assume responsibility for biowarfare research and development under the supervision of the War Research Service. Subsequently, the Army chose Camp Detrick in Frederick, MD, as the site for the biowarfare research program, and construction began in April 1943. The emphasis of the program was protection of soldiers. To achieve this goal, CWS created the Special Projects Division (SPD). The SPD built and operated numerous of facilities, including Camp Detrick in April 1943 with the parent research and pilot plant; Field Testing Facility in Horn Island Mississippi in June 1943; Vigo Ordinance Plant in Terre Haute, IN in May 1944; Granite Peak Test Site at Dugway Proving Grounds for field testing in June 1944; and Fort Terry in Plum Island, NY for Veterinary Testing in 1944." [https://sci-hub.ee/https://link.springer.com/chapter/10.1385/1-59259-764-5:155] The book chapter didn't say anything specifically about brucellocis tests in 1944-1946, even though the chapter was titled "Medical Protection Against Brucellosis", which may have led to confusion about the tests being specifically about brucellosis.

Wikipedia says that Fort Terry was "working on veterinary testing in connection with the weaponization of brucellosis", which features the same phrase "veterinary testing" that was used in the book chapter. When I googled for a combination of the terms "veterinary testing" and "Fort Terry" in double quotes, all results were about the Wikipedia article or the book chapter, so it's likely that the Wikipedia article relied on the book chapter as a source. The somewhat vague wording of "in connection with the weaponization of brucellosis" might indicate that the exact relationship between the tests and brucellosis was unclear to the author of the Wikipedia article (as it would have been based on the book chapter, which did not even specify if the presumed tests performed at Plum Island involved brucellosis or not).

The book chapter was part of a book about biological weapons edited by authors at Fort Detrick, and the first author of the chapter was the head of the US Army's brucellosis vaccine program. So the book chapter seems like a credible source, but it's still possible that the authors would have confused the use of Plum Island as a veterinary research site in the 50s with SPD-era activities in the 40s, because I didn't find any other source which backed up the claim that Plum Island was employed as a veterinary testing site under the SPD. Grok also said:

The only primary reference to Fort Terry (Plum Island) being part of the U.S. Army Chemical Warfare Service's Special Projects Division (SPD) during WWII is a single planning-level list from a 2005 book chapter. No declassified documents, official histories, or operational records show that Fort Terry was actually used for biological warfare (BW) research, veterinary testing, or any SPD activities in 1944-46. It remained a coastal defense/anti-submarine site during the war and was largely inactive afterward until its reactivation for anti-animal BW work in 1952.

[...]

Reliable histories, declassified summaries, and site-specific records show:

Fort Terry/Plum Island is never mentioned as an active or operational BW site in these accounts. SPD activities largely ceased by August 1945.

The biological warfare testing site at Horn Island opened in 1943 and closed in 1946. [https://en.wikipedia.org/wiki/Horn_Island_Chemical_Warfare_Service_Quarantine_Station] The reason why the Wikipedia article about Erich Traub says that "Plum Island was part of the U.S. biological warfare program in 1944-46" might be that operations on sites like the Vigo Ordnance Plant and Horn Island had ceased by 1946, even though the SPD was already ordered to cease operations in August 1945.

The primary biological test site overseen by the SPD was Granite Peak Installation, which was part of the Dugway Proving Ground CBW testing site. Granite Peak was officially deactivated and closed in 1945, even though it was reactivated during the Korean war, and in 1952 the Army Chemical Corps performed a test at the site on brucellosis in guinea pigs. [https://en.wikipedia.org/wiki/Granite_Peak_Installation] The Dugway Proving Ground had become inactive by August 1946, even though it was later reactivated in 1951. [https://en.wikipedia.org/wiki/Dugway_Proving_Ground] The website of Dugway Proving Ground says: "DPG underwent a temporary deactivation at the end of WWII, but in 1950, with the beginning of the Korean War, interest in CBW was rekindled. In 1951, CBW divisions were activated at DPG and a flurry of construction was begun." https://web.archive.org/web/20100713065300/http://www.dugway.army.mil/index.php/index/content/id/83]