Clarification on the Lyme Borreliosis Clade and its relationship to Borrelia anserina

Why Bacterial Phylogeny is Only a Rough Guide and Not an Absolute in Sophisticated Man-Made Conditions Spanning the Globe

Recently, a critic, after “asking Grok,” has tried to cast doubt on the idea that Borrelia burgdorferi and the rest of the Lyme Borreliosis clade of the Borrelia genus could have come from Borrelia anserina, nor have been engineered in the span of just several years, claiming that millions of years of evolution separate them. Its understandable that this would seem to be the case at first glance, even for wise ol’ Grok, and for those not realizing that bacterial phylogeny can only be used as a rough guide, and before unpacking the highly unusual conditions and techniques that Erich Traub was using and developing, first in Germany under their tick and insect simulant program, then shared with the Japanese and duplicated there, duplicated again in Russia after the capture and acquisition of Insel Riems, and finally, brought to the United States, duplicated again in North America, who then shared it with Britain, Canada, and possibly Australia, duplicating it yet again there.¹

By “duplicating” I mean the same practice - repeated rearing and inoculating of tick vectors and packing them with a myriad of viral, mycoplsmal, bacterial, and rickettsial pathogens and releasing them into the environment - something that never would have happened under natural conditions and thus cannot be seen through the eyes of natural evolution by any stretch of the imagination. This brings highly unusual man-made conditions that span globally taking each their own evolutionary path in their respective ecosystem, and no studies in phylogenic evolutionary relationships have ever considered and incorporated such elements into the arrangement of bacterial phylogenies.

In saying that Lyme disease was closest to the avian relapsing fever Borrelia anserina, I need to clarify that I meant the entire Lyme Borreliosis clade,² but apparently I was not clear enough in making that point so there has been some confusion. Borrelia burgdorferi is obviously closer to some of its sibling species in the Lyme Borreliosis clade, like Borrelia afzelii, Borrelia garinii, among others others, which Borrelia anserina served as an outgroup. I am saying the entire Lyme clade came from Borrelia anserina and it was engineered in just a few years through highly unique and sophisticated conditions that bypass natural evolution and create conditions that have never been openly studied in the context of a man-made phenomenon. This is especially unique when the ticks carrying such a sophisticated mix of new infections are then introduced into many new climates across the globe by man - determined to advance their biological warfare capabilities and biodefense programs on multiple parts of the globe simultaneously.

It does not mean Traub engineered each species of the clade himself, it could have been just one or two species that when shared with other superpowers or introduced into different climates or ecosystems - rapidly evolved due to the unusual nature of the multiple pathogens it was growing with in new vectors that are immune tolerant, along with co-infecting mycoplasma and bacteriophage varieties. It is known that viruses rapidly mutate in the immunosuppressed and this could also create highly unusual conditions for unprecedented rapid evolution of bacterial pathogens into what appear to be new species and sub-species evolving from just one species - Borrelia anserina - in a short amount of time, and yes, a span of just several years, not hundreds, thousands, or millions of years. We are talking many jumps in a short timeframe - new tropisms, hosts, vectors, and resistance genes to antibiotics. These are all traits that Traub specialized in and added to its engineered evolution. Taken together, this could completely remodel a species into entirely new clades separated by what appear to be long-term evolutionary distances when in fact it was very short-term changes in sophisticated growing conditions enabling diverse mutations and rapid evolution that when released in diverse ecosystems across the globe, would further evolve in highly unique and unprecedented ways.

However, it brings up an important point; we only use bacterial phylogeny as a rough guide in reconstructing the split between the Lyme Borreliosis clade and Borrelia anserina in the context I put forward in The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare. But this rule of thumb is also true for all scientists to go by. The phylogenic tree should never be treated as a fully conclusive end all be all. It is not an absolute, and in fact there are many elements that can skew the phylogenic data. In this article, I will explain in greater depth why that is the case, and why such unusual man-made adaptations coupled with sophisticated growing environments could have allowed for rapid transformation and evolution of the Borrelia anserina pathogen to give the appearance of multiple species across the globe whose genetic profiles seem much further in distance between the species than they actually were.³

My book’s evidence does not document every step and provide hard evidence on each point along the way showing how this was done. My job is to look at the big picture of a highly secretive and sophisticated form of warfare with microbiology and reverse engineer the story based on available evidence and testimony, just as a scientist would do in recreating long-term evolutionary history. I rely on the extensive, overlapping circumstantial evidence in toto to make my case, thus, in a way that explains the entirety of the picture without contradiction, and by doing it this way - it leaves a far more solid tapestry based on available evidence than by relying on bacterial phylogenies alone which are also built on theories and inferences that are anything but absolute and assume no man-made conditions or anomalies were involved other than steady long-term evolution in a natural habitat over millions of years. We know this to be wrong when looking back at the history of the biological warfare race.

The entire study and assembly of bacterial phylogenic trees has been done in times where man was heavily influencing the environment and studying microorganisms in controlled laboratory conditions, so to look at phylogeny as a concrete marker of natural evolution would be almost ridiculous when you take into consideration how much influence we have had on environments and microbes since modern science began. They’ve never had control samples to compare to when microorganisms were actually thriving in a natural habitat free of man-made influence and controlled laboratory conditions.

Many scientists have even argued that bacterial phylogeny as an evolutionary tree is insufficient and must be uprooted as a model because bacterial lifeforms are chimeric, they are subject to Horizontal Gene Transfer (HGT) inheriting DNA and genetic material from unrelated bacteria, and even the so-called stable 16S rRNA operon used as the gold standard for reconstructing bacterial phylogenies is far more malleable than initially thought. The 16S rRNA operon is in fact amenable to Horizontal Gene Transfer,⁴ which means you can’t depend on phylogenic trees alone and shows its limitations to be significant, as the 16S rRNA gene is much more prone to rapid evolutionary changes the prokaryotes are than the higher forms of life such as mammals that undergo sexual reproduction and vertical gene transfer. Therefore, making the analogy between the distance of man and chimps compared to bacteria simply does not work here.

Especially noteworthy is that giving bacteria antibiotic resistance genes can mutate the 16S rRNA genes considerably and there is some evidence that suggests Traub was already adept at working with such environments and we know this to be an important target for biological warfare research and development. Another limitation in solely relying on the phylogeny is that there was no sequencing of the earlier strains used, such as the Borrelia anserina that Werner Schäfer and Erich Traub began maintaining in 1939 from Franz Jahnel.⁵

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),⁶⁷ 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.

Absolutely none of this type of unusual man-made biodefense activity was factored into the equation by academic researchers reconstructing bacterial phylogenic trees, making an already limited theoretical framework vulnerable to be skewed a thousand ways to Sunday. We like to think that we can just go to GenBank and see definitive ancestral relationships, timelines, and evolutionary distances - when in fact this is not necessarily the case.

We need to also consider all the additional evidence - as well as the underlying motivations showing the desire and intent to modify specific agents like Borrelia anserina were present. A growing demand to completely remodel the pathogen, change its pathogenic properties, tropisms, adapt it to new hosts, add antibacterial resistance genes, all as far back as in the days of WWII. Borrelia anserina is a case in point, because there was a growing demand to do this to Borrelia anserina in pre-WWII Germany at the time.

As is common in top secret research and development, advances in science were often known many decades before their public disclosures. I believe Insel Riems and the Germans were already up to speed on current modern-day bioengineering back in the days of World War II, as Insel Riems was working with several bacteriophage varieties and Mycoplasma. Both would act to shuttle genes between the different cocktail of pathogens and accelerate rapid evolution. I believe adding bacterial resistance was already a known skill by Erich Traub. Perhaps this is why his son Walter then went on to spend his entire life studying antibiotic resistence in simulant strains of bacteria like Serratia marcescens.

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:

a) natural retrogression and termination of epizootics;

b) increase in potency of the causative agent;

c) virus adaptation to certain species of animals and escalation or decrease of infectivity and pathogenicity for other species;

d) different affinity of virus strains for certain cells (cardiac FMD);

e) differences in susceptibility among individual animals of the same species;

f) reduced susceptibility in undernourished individuals;

g) different behavior of different virus types;

h) persistent infection;

i) serological variation.¹⁰

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.¹¹

Remodeling Borrelia anserina: A Growing Demand in Nazi Germany

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.

Erich Traub had a specialty in the art of adaptation, and he was involved in having an Insel Riems associate Hans Cristoph-Nagel adapt FMD Virus to mice, completely changing its qualities to become highly neurotropic,¹³ turning it into a central nervous system disease after the 140^th+ passage when it previously was a disease that caused blisters on the mouth and hooves of cattle.¹⁴ This adaptation occurred when Traub visited the Insel Riems facility on a return visit from the Rockefeller Institute in the years 1936-37 and brought mice from the Rockefeller Institute to Nagel, likely infected with the LCM virus and served as a helper virus to assist the change.¹⁵ Traub then adapted FMD Virus to chicken eggs when no one else had been successful in their attempts. He did this by mixing 12 different variants of FMD Virus in one egg and alternating passages between the egg and guinea pig to get the virus slowly used to the egg until it was fully adapted to the egg.¹⁶

In 1936, a German researcher Margeret Zuelzer had found a new vector for Borrelia anserina in the Culex mosquito,¹⁷ so there was an obvious demand not only to change its host and tropisms to be more like syphilis, but to also find new vectors to transmit the spirochete. Taken altogether, this would require a total makeover of the pathogen which could have easily mutated the 16S rRNA operon which the phylogenic trees are assembled based on under the false assumption that they are immune to horizontal gene transfer.

The next important part of this timeline is when Erich Traub was gaining unique tick-borne disease expertise as assistant professor to Dr. Karl Beller in 1939. In a chapter Heartwater and other animal rickettsioses (Herzwasser und sonstige tierische Rickettsiosen) from the Handbook for Viral Disease (Handbüch der Viruskrankheiten) published in 1939 by Karl Beller, he studied complex systems of multiple infections (Babesia, Bartonella, Ehrlichia, Rickettsisa, and Leishmania) all rolled into one host and had the foreknowledge that it was possible to transmit relapsing fever spirochetes through hard-bodied ticks like the brown dog tick.¹⁸ Since Erich Traub was working with him at the time as assistant professor he would have gained expertise from Beller’s studies of tick-borne disease. We later find all the same co-infections infecting hard-bodied Ixodes ticks in Europe and North America when he was brought to the United States in Project Paperclip, and not long after that the Lyme explosion began. He merely swapped Leishmania with a completely remodeled Borrelia anserina. This interesting chapter demonstrated that when such a complex of multiple overlapping co-infections were produced, it caused immune tolerance, which had sometimes been called prämmunity.

This would most likely be true for the tick as well, where a tick carrying multiple overlapping pathogens from foreign sources is immunosuppressed by the cocktail of infections. It is known that viral mutations happen rapidly in immunosuppressed hosts,¹⁹ and this would create a synergistic effect for the spirochetes and other co-infecting pathogens. No one has ever studied how this affects the evolution of specific pathogens in relation to assembling bacterial phylogenic trees. Therefore, the bacterial phylogeny of the Lyme Borreliosis clade of Borrelia cannot be seen through the lens of natural evolution and its rapid evolution is vastly different than than that seen in any kind of basic serial passage of a single species of microorganism grown on their own in a single type of animal.

Insel Riems was a state-of-the-art facility at the time and had been doing work on mycoplasma and bacteriophages, and they had the capability to completely remodel Borrelia anserina as was in growing demand at the time. It was known that Germany was conducting all the same simulant tests in WWII that Traub would later supervise in the United States, as Kurt Blöme’s file shows.²⁰ The Germans had actually started this kind of testing in the subways of London and Paris in the 1930s.²¹ It is also very likely that the Japanese duplicated these tests as they were sharing at least some of the important chemical and biological warfare intelligence,²² and this is why the Lyme clade includes some species from Japan. Traub and Karl Beller had been citing Japanese research using different insects to transmit Equine Infectious Anemia Virus in 1942.²³

The Soviet Union captured Insel Riems in 1945 and hauled off the majority of their lab equipment and research records that was done up to 1945,²⁴ so the Soviet Union would have certainly been further developing and testing this unusual cocktail of infectious disease in vectors in the Soviet Union,²⁵ further diversifying the lineage of remodeled Borrelia anserina – the Lyme Borreliosis clade coming from Borrelia anserina as an outgroup.

Project Paperclip and Plum Island Work

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 and even before he was brought to the USA the congressional record shows that they were planning on having him working at Plum Island under the law that established the laboratory for work on FMD and foreign animal diseases when they mentioned him in the hearing, not by name, but by other recognizable elements to reveal his identification, such as calling him the world’s top specialist of FMD, but they said he had applied for work in the West but was rejected for his Nazi affiliations and returned to the Russian zone, which is exactly what happened to Traub before Soviet moles in MI6 facilitated his phony “escape” in 1948.²⁷

Erich Traub filled out an application to lead Plum Island in 1958, initially I thought this was a security investigation to visit the United States as he was attending a virology conference that year, as the second half of the title of the form “for Sensitive Position” was nearly illegible. He cited the public law 496 80th congress - establishing an FMD lab - as the reason for appointment and that hearing in 1948 spoke about putting Traub there directly even if not by name. Plum Island was used for veterinary testing since at least 1944,²⁸ so it would have been a desirable place to conduct anti-animal tests and he would have been involved in any work there from his earlier days in Paperclip.²⁹

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.

Furthermore, a paper Traub co-authored with Lawrence O. Mott from the USDA on Vesicular Stomatitis, published in 1958, shows that Traub was working with the USDA at the Beltsville station of the Agricultural Research Service (ARS) which at that time would have been the Bureau of Animal Industry (BAI). At the bottom left of the paper, it states the work was done in 1950 at the USDA facility. Lawrence O. Mott was also very involved with the tick program and attended conferences on Anaplasmosis. Therefore, it shows Traub was working with USDA officials and at their facilities working with one of the USDA officials (L. O. Mott) who was involved with the tick programs:

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.³⁰

They said they were rearing infected ticks at the time, and although I failed to make this connection in my book, its recently become apparent to me that Traub may have been selling American biodefense on the idea that these Russian-doll cocktail infected ticks could have served as vectors to inoculate the population with a live bacterial vaccine for poultry, livestock, and humans against a multitude of different foreign diseases. He was back and forth between Colombia in South America and the Northeast United States from 1949-1952,³¹ loosely in parallel with the bird migration patterns.³²

We know Erich Traub was intended to work on arthropod-borne disease since the file for his German female lab tech Anne Bürger proves it as she was to maintain rickettsial pathogens in serial passages:

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.³³

It also proves they were the most skilled at what they were doing and no one else had the sophisticated level of skill and understanding that Traub and Bürger had:

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.³⁴

In fact, there were no top-rate scientists in America that could replace them and Traub himself was the most prized scientist in the global biological weapons race:

Dr. Traub is an eminent virologist and an authority on matters pertaining to biological warfare. His assignment to the Naval Medical Research Institute will fulfill an urgent need that cannot be met by personnel available in United States. His probable knowledge of preparations for biological warfare in other countries renders mandatory every effort to secure his services.³⁵

Traub was listed as a supervisory bacteriologist in his intelligence file, so he was clearly overseeing simulant tests, routine at the time and which were learned from being advised by the Nazis in Paperclip since that’s how they ran their biodefense program, and most likely the simulant tests were a covert vaccination program using open-air germs and insect vectors like ticks and mosquitoes. We have the source in Lab 257: The Disturbing Story of the Government’s Secret Plum Island Germ Laboratory discussing the section of the island where Traub was said to be releasing the ticks, but we also have a later publication showing abandoned tires still dotted the landscape from earlier tests on the island in a survey conducted and published in a 1980 issue of Mosquito News, “Aedes atropalpus Breeding in Artificial Containers in Suffolk County, New York.”³⁶

What makes me think Traub may have been selling the tick and mosquito simulants as a vaccine program is because he used to refer to immune tolerance as infectious immunity and the multiple overlapping infections produce exactly that.³⁷³⁸ In my book I talked about how Vaccinia virus was cleared as a standard simulant to be used in open air tests by the 1950s,³⁹ and back in 1940 Erich Traub gave the simulant bacteria Serratia marcescens properties of bovine papular stomatitis virus, a poxvirus very closely related to Vaccinia.⁴⁰ In the 1990s, these simulant tests were still going on, and it makes no sense to continue spreading bacteria in open-air tests for decades “just to see how it spreads out.” It makes more sense as a covert vaccine program done routinely without our knowledge or consent, and indeed they were looking at what vaccine viruses could be used as standard simulants by the 1990s.⁴¹

In 2012, NIH was still trying to sell the idea of immune tolerance as a defense strategy,⁴² which indicates that they were looking at immune tolerance as an acceptable immunity all along since the days of Traub, just as today we are talking about vaccinating the population with mosquitoes released into the environment.⁴³

Plum Island Was Chartered to Handle Foreign Animal Diseases like Lyme Disease and its Co-Infections, so Why Didn’t They?

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.⁴⁴ We can see that such a statement is actually a blatant lie - they published a 1961 paper on subclinical Leptospirosis of cattle.⁴⁵ Leptospira is a spirochete and Plum Island did work with other tickborne diseases like heartwater (Cowdria ruminantium) and Theileria parva.⁴⁶ There was a notable paper on early Lyme cases isolating Leptospira spirochetes from the bullseye rash of Lyme patients, and they ignored its significance because it did not produce a robust antibody response, which would be expected since Leptospira is very immunosuppressive.⁴⁷

Dr. Breeze also told Jesse Ventura in an episode of Conspiracy Theory that he did not know who Erich Traub was when asked.⁴⁸ This would be inconceivable as anyone with deep experience in the field of virology and FMD virus would have known who Erich Traub was, especially since Roger Breeze was a former roommate of Robert Shope, the son of Traub’s American mentor who had dinner with Traub in the late 1970s.⁴⁹ This is telling because it shows defensive behavior and intentional dishonesty coming from the director of Plum Island toward anything related to Lyme disease, tick-borne disease, and Erich Traub.

But what is more telling than the intentionally misleading statements is 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.⁵⁰ It shows serious incongruency and such anomalies need explaining. It would be like if a shootout happened in a certain jurisdiction and the police just left it for the town hall to deal with.

This is especially noteworthy since several top Plum Island officials had attended the earlier 1953 poultry conference on biowarfare on the poultry industry discussing avian spirochetosis as an agent of special concern.⁵¹ It stated that they believed several foreign animal diseases had already gained entrance into the U.S. and a bioterrorist using multiple overlapping infections in the same host was one method that could be used against them, exactly what Traub was doing. Lyme disease is carried by a multitude of birds and can affect land animals, and that makes the safety of the poultry industry a clear and present concern.

From the early 1950s to the 1960s there were several outbreaks of Borrelia anserina across the United States, and in one paper on an outbreak in Arizona from 1960 thanks William Hinshaw of the Fort Detrick U. S. Biological Warfare laboratories – which shows that biowarfare specialists had a clear interest in this pathogen.⁵² Especially noteworthy are the attempts to study its “carrier state” in chickens,⁵³ and in the immunosuppressed.⁵⁴ Were they expecting it to suddenly turn from a highly fatal disease to an avirulent pathogen? What would give them that idea? Was it because Dr. Traub had been selling them on the idea of immune tolerance as a vaccine to impart an infectious immunity? That he could make an avirulent vaccine strain of Borrelia anserina mixed with other foreign tick-borne diseases which he could then use in the insect simulant program as both a tracer and a vaccine?

These simulant tests appear to have continued all the way up to the present day as an integral part of biodefense activities. There is no evidence to suggest they ever stopped. Interestingly, a document from the early 90s shows they were not only still assessing what pathogens they could use as standard simulants, they were looking at what vaccine viruses they could use, lending more weight to the simulant program being a covert immunization program done without our knowledge or consent.⁵⁵ Calling it a standard simulant implies it is routinely done, and surely they would have figured out the dynamics of “how it spreads out” by the 1950s, but this was a probably just a cover to hide the fact they have been attempting to immunize us without our knowledge or consent all this time.

Despite adequate backlash by concerned citizens about the human rights violations that occur by testing on the population without their knowledge or consent, the government still struck these concerns down and ruled that the tests were indispensable to biodefense. The fact that Vaccinia virus was cleared as a safe simulant in the 1950s yet excluded by the 1990s due to its dangerous potential shows the gap in safety assessments:

1950s:

UK outlined the work done on vaccinia, emphasizing that this was very much an interim report. Because vaccinia was relatively safe, easy to produce and easy to assess, it was used as a simulant in both laboratory and field trials in order to gain in formation on the use of smallpox virus (Variola) as a [biological warfare] agent.⁵⁶

1990s:

Despite its extensive use for immunization of the human population against smallpox, vaccinia virus is a virus of relatively high pathogenicity with a long, if sporadic history of lethal infections and postvaccinial encephalitis. Even more serious than the standard complications listed in the Submission is the prospect of vaccinial pneumonia in a population now almost devoid of the individual or herd immunity resulting from smallpox vaccination. Vaccinia virus must unquestionably, therefore, be excluded.⁵⁷

I wonder how many injuries or deaths had to occur before they realized the shortcomings of their earlier assessment that it was safe? This re-assessment from the 1990s was also looking at new live agents and vaccine viruses that could be used as standard simulants and serve as replacements to Vaccinia, citing poliovirus, Newcastle disease Virus, measles, mumps, and rubella. This is highly alarming and erodes the fabric of basic human freedoms that we should have a say in.

After learning what immune tolerance is and how it destroys health, brings neuropsychiatric disorders, and cancers, it is beyond criminal to remove someone’s right to be free from such health-destroying agents unleashed upon us without our knowledge or consent. It totally undermines the idea of a free society, of bodily autonomy, of informed consent. It puts us back in the conditions of Nazi Germany and the Soviet Union.

Subclinical Leptospirosis in cattle being studied by Plum Island Animal Disease Center shows they were probably conducting testing with live bacterial vaccines that induced immune tolerance as an infectious immunity rather than the so-called sterile immunity where the pathogen is cleared. This infectious immunity, or immune tolerance, comes with serious long-term often irreversible side effects and poor quality of life in the future. It also comes with death via cancer and wasting disease – an indirect but more painful and agonizing way to die since it is so prolonged and slow.

Traub probably got full approval by American biodefense to conduct these tests if he was selling them on the idea of disease tolerance as a form of immunity. This would indicate he was rearing these ticks with multiple pathogens as live bacterial multi-valent vaccines. In 1961, they were putting forward the idea of using immune tolerance in vaccination campaigns to keep the poultry industry afloat.⁵⁸ Even in more recent times (2012) they were still trying to sell disease tolerance as an acceptable form of immunity.⁵⁹ We have obviously learned nothing from the harm caused by the simulant program. Now they are probably trying to create vaccines to protect against earlier “vaccines.”

However, not to get too far off track, my point in discussing this activity in America is to show that highly sophisticated conditions for multiple pathogens in tick vectors would have been once again at play on the North American continent, and 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.⁶⁰ 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.

Literature on Borrelia anserina is extremely limited compared to Borrelia burgdorferi, and no sequencing of the spirochetes or any other co-infecting pathogens maintained by Schäfer, Traub, or Beller from that time were ever conducted. Add this to the complex, sophisticated environments they were placed in. Conditions, fair to say, that have never been considered as man-made bioengineering and directed evolution. They found all these species in the Lyme clade and no one can say with any certainty that these aren’t very recent events considering the global spread of the pathogen.

Because of Horizontal Gene Transfer (HGT), chimerism, and the complete absence of modern ethical open source studies to replicate the high-density, multi-pathogen, bacteriophage and mycoplasma-facilitated cocktail in the Ixodes or other ticks across vastly diverse climates has never been considered in the construction of phylogenic trees by academic researchers. It shows us that standard phylogenetic trees do not necessarily account for the very sophisticated man-made influences at work. This would be especially true regarding the Lyme Borreliosis clade having descended from Borrelia anserina as a very recent event, undergoing rapid evolution in a short time frame, across multiple points of the globe, each with their own unique ecosystem, creating what appears to be long-term evolutionary distance spanning millions of years between the evolution of new species, when in fact it was just several years of sophisticated man-made evolution.

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).⁶¹ Taken together with the presence of the highly conserved flagellar epitopes shared between Borrelia anserina and Borrelia burgdorferi,⁶² and the fact that birds serve as immune tolerant carriers of Borrelia burgdorferi,⁶³ this reflects very close relationships, far more powerful than relying on the phylogenic tree alone as a deciding factor. Especially when we add in all of the manmade elements that would have contributed to the rapid evolution of Borrelia anserina brought to many corners of the globe and packed into ticks with multiple overlapping co-infecting agents, mycoplasma, viruses, and bacteriophages.

From the 1995 paper by Hovind-Hougan discussed above on A morphological characterization of Borrelia anserina, clearly comparing Borrelia burgdorferi to Borrelia anserina showing striking similarities:

both of the above image are from : Hovind-Hougen, K. “A Morphological Characterization of Borrelia Anserina.” Microbiology. (Reading, England). U.S. National Library of Medicine, January 1995. https://www.ncbi.nlm.nih.gov/pubmed/7894723

But Richard Marconi had in fact put forward in his paper that the Lyme Borreliosis clade descended from Borrelia anserina, which served as an outgroup. If Traub and other colleagues (whether Germans, Russians, Americans, Iranians, and so on) had been restructuring the spirochete for multi-system changes such as interspecies transfer or adaptation, changing tropisms, and giving it highly unusual growing environments like the Russian-doll cocktail of overlapping infections in a single vector, with additional horizontal gene transfer through mycoplasma and bacteriophages to shuttle a sophisticated network of genes between the agents, this new clade would be exactly what one would expect to see.

The fact that all the way up to 1951 the black-legged tick was not listed as a transmitter of any known human disease, but then suddenly has multiple overlapping human diseases all rolled into the same vector within a decade is highly unusual. However, if seen through the lens of the story in The Sleeper Agent, it makes sense that they would have began using the black-legged tick for such insect simulant tests, and the USDA was collecting black-legged ticks off animals on a routine basis according to Andrew J. Rogers in his 1951 thesis A Study of the Ixodid Ticks of Northern Florida, Including the Biology and Life History of Ixodes Scapularis Say (Ixodidae: Acarina).⁶⁴

Therefore, to say that Borrelia burgdorferi and the Lyme Borreliosis clade of Borrelia could not possibly have come from Borrelia anserina in just several years based on the phylogenic tree data alone is jumping the gun and oversimplifying the situation to reflect an assumed natural evolutionary phylogenic tree when quite the contrary is true. These were exceptionally unique and highly sophisticated conditions and environments overlapping that could have easily transformed the pathogen into what seemed like an entirely separate clade - the Lyme Borreliosis clade - and all from one species that was remodelled perhaps several times and continued to undergo rapid evolution on different parts of the globe in the span of just a few years.

Again, I have never claimed absolute proof of every step of the way, I’ve been looking at the big picture and rebuilding the storyline until there are no contradictions. So far the totality of what I present fits the picture exactly without contradiction based on available data, and I present my case as one would do in a court of law, and I believe I have made my case beyond a reasonable doubt which I presented to the public in my book The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare.

After schooling Grok on the complexity and sophisticated elements involved in this biological weapons race, the LLM realizes that its responses to Henshit’s questions were lacking and often incorrect, as the LLM’s expertise does not match my own many years of study and it acknowledges its mistakes:

Grok’s advice for Henshit:

Suggested reading

---

Revisiting bacterial phylogeny: Natural and experimental evidence for horizontal gene transfer of 16S rRNA

https://pmc.ncbi.nlm.nih.gov/articles/PMC3661144/

Phylogenetic classification and the universal tree

https://pubmed.ncbi.nlm.nih.gov/10381871/

Seeing the Forest for the Trees: The Limitations of Phylogenies in Comparative Biology.

https://www.journals.uchicago.edu/doi/pdf/10.1086/660020

Horizontal gene transfer in evolution: facts and challenges

https://pmc.ncbi.nlm.nih.gov/articles/PMC2842723/

Uprooting the tree of life

https://pubmed.ncbi.nlm.nih.gov/10710791/

Uncoordinated phylogeography of Borrelia burgdorferi and its tick vector, Ixodes scapularis

https://pmc.ncbi.nlm.nih.gov/articles/PMC2919648/

Identification of novel insertion elements, restriction fragment length polymorphism patterns, and discontinuous 23S rRNA in Lyme disease spirochetes: phylogenetic analyses of rRNA genes and their intergenic spacers in Borrelia japonica sp. nov. and genomic group 21038 (Borrelia andersonii sp. nov.) isolates

https://pubmed.ncbi.nlm.nih.gov/7494041/

Footnotes

1. A. W. Finnegan. The Sleeper Agent: The Rise of Lyme Disease, Chronic Illness, and the Great Imitator Antigens of Biological Warfare. TrineDay. (Oregon 2023)

2. Marconi, R. T., Liveris, D., & Schwartz, I. (1995). Identification of novel insertion elements, restriction fragment length polymorphism patterns, and discontinuous 23S rRNA in Lyme disease spirochetes: phylogenetic analyses of rRNA genes and their intergenic spacers in Borrelia japonica sp. nov. and genomic group 21038 (Borrelia andersonii sp. nov.) isolates. Journal of clinical microbiology, 33(9), 2427–2434. https://doi.org/10.1128/jcm.33.9.2427-2434.1995

3. Borin, J. M., Lee, J. J., Lucia-Sanz, A., Gerbino, K. R., Weitz, J. S., & Meyer, J. R. (2023). Rapid bacteria-phage coevolution drives the emergence of multiscale networks. Science (New York, N.Y.), 382(6671), 674–678. https://doi.org/10.1126/science.adi5536

4. Kitahara, K., & Miyazaki, K. (2013). Revisiting bacterial phylogeny: Natural and experimental evidence for horizontal gene transfer of 16S rRNA. Mobile genetic elements, 3(1), e24210. https://doi.org/10.4161/mge.24210

5. Schäfer, W. (1939). Fortführung von Spirochaeta gallinarum-Stämmen von Eipassagen. [The Maintenance of Spirochaeta gallinarum by Passage in Fowl Embryos.] Vet. Bull., 11, 220. [translated by A. Finnegan 2019]

6. RUSKA, H., & C. MENZE: Die Größe von Typhusbakteriophagen nach der Filtrationsendpunktbestimmung und dem elektronenmikroskopischen Bild. [The size of typhus bacteriophages after the final filtration point determination and the electron microscopic picture.] Kolloid-Zeitschrift 110 (1948), S. 103-105

7. RUSKA, H: Zur Frage der Potenzierung von Bakteriophagenlösungen durch Zerschäumen [On the question of the potentiation of bacteriophage solutions by foaming]. Kolloid-Zeitschrift 110 (1948), S. 175-177 [paper submitted in 1945, not published until 1948.]

8. Traub, E., Schneider, B., Zuchtung des Virus der Maul- und Klauenseuche im bebruteten Huhnerei. [Breeding of the Virus of Foot-and-Mouth Disease Virus in Chicken Embryos]. Z Naturforsch B. May-Jun; 3 (5-6):178-87. (1948) [Translated to English by A. Finnegan (2019)]

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10. Traub, E., Kanhai, G. K., & Kesting, F. (1968). Behavior of foot-and-mouth disease virus on serial passage in different kinds of cells. A contribution to experimental epidemiology at cell level. Zentralblatt fur Veterinarmedizin. Reihe B. Journal of veterinary medicine. Series B, 15(5), 525–539. https://doi.org/10.1111/j.1439-0450.1968.tb00327.x

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