Lyme Rouleaux: Covert symptom or clue to something more?

Let’s rouleaux the dice and see what we’ll get…

“What the heck is that?” my friend asked when she observed the photographic results of my blood smear under live microscopy. “That’s rouleaux” said the certified microscopist (pronounced roo-low).

“Sticky” blood is something about which I had heard years ago when it comes to Lyme disease patients. Hyperviscosity is a process which allows the red bood cells (RBCs) to stick, and to stack together because of their discoid shape. Some laboratory scientists refer to this condition as hyperviscosity, and it is a term used in both the laboratory to describe this sticky blood, and also in the garage to describe thick fluids. I guess I needed an oil change.

There are many causes of this blood anomaly, (rouleau singular, aux-plural) so don’t dial 9-1-1 just yet. Some artifacts of this type will be found under the microscope, but when they are predominantly stacked in this coin-like manner, you may find increased proteins, globulins (antibodies), increased ESR (erythrocyte sedimentation rate) or sed rate; and increased fibrinogen (from the liver, and converted into fibrin then linked to factor XIII to form clots). Now all this is just terrific as long as you don’t know what it means.

Put simply, rouleaux may be seen as an artifact, or it may be found in Multiple myeloma and other cancers, in inflammatory conditions, connective tissue disorders, cryoglobinemia, sarcoidosis, cirrhosis, diabetes, and Waldenström’s disease. It is also seen in people who are anemic, and in “Lyme disease” patients. I put the disease in quotes because the longer I study this infectious disease complex, the more convinced I am that we are dealing with multiple factors. Oh sure you will say that a Lyme patient has Borrelia burgdorferi (“Bb”) spirochetes and “co-infections.” Many Lyme patients will rattle off the top five, including Rocky Mountain Spotted Fever, Babesia, Bartonella, Ehrlichiosis, and various Typhus strains (rickettsiae). A few well-read patients will include Q-fever or Brucellosis to the differential. But don’t you want to know there are a host of other intracellular infections that can come along for the ride, and many of them you will learn about in my Lyme books.

What makes up the Bb spirochete is still somewhat of a mystery, although I attempt to decipher its exact and regionally variable composition in my two latest tomes God Science: The Secret World of Rampant Genetics, Hidden Illness, and Biotech Profiteering, and The Fourth Monkey: An Untold History of the Lyme Disease Epidemic ( or Amazon). In those books I have painstakingly identified through a massive brain upload of various research texts, what I feel makes up the outer surface proteins (Osp) A, B, and C of the Bb spirochete. I also speculate with supportive research, about the rest of this spiral-shaped bacterium, as well as its historical origins — and the answers are far different than what the public (and scientific) sectors have been told.

Indeed in the early days of the “juvenile arthritis” outbreak of the late 1960s-early 1970s, Connecticut Rheumatologist Dr. Allen C. Steere and pals were busy studying what are called cryoprecipitates (cryoimmunoglobulins) or “cryo”. These studies may not have been a coincidence. This condition is felt to be associated with the clinical involvement of skin and joints in Lyme disease cases. Cryoimmunoglobulins are serum antibodies that were being studied by scientists who were investigating the outbreak of Lyme disease in Connecticut. This is important because viruses and bacteriae have been implicated in forming cryoimmunoglobulins (essentially sticky antibodies), and therefore are felt to be contributors to rheumatic diseases including Rheumatoid Arthritis, and Lyme disease.

If the scientists were concerned that infectious agents were causing Lyme “arthritis”, it may explain why they tested Connecticut patient serum samples against infectious agents including insect arboviruses (arthropod-borne viruses), and against other spirochetes the (animal) leptospires, and at least one kind of plant spirochete, the spiroplasma. Each of these agents are commonly found inside the bodies of ticks and other arthropods and insects, although you may never be told about some of these buggies, whether you have been diagnosed with, or suspect you have RA or Lyme disease. In fact the Bb spirochete of Lyme disease may be an aggregate, or a collection of microbes and their genes, and contain a mutated leptospira, an insect virus, and a spiroplasma. Case in point, there is a “B31” strain of Bb spirochete, and there is a “B31” spiroplasma as well. (To learn more about this, see my latest books.)

But back to cryoprecipitates. These also appear in a frozen blood product that is prepared from human plasma. This is used as a blood clotting agent for hemophiliacs, and is also known as cryoprecipitated antihemophilic factor or “cryo.” Depending upon blood type, the product will contain antibodies to the blood type from which it was made.

The reference to this in Lyme-related articles that were co-authored by Dr. Steere and friends may suggest that there was evidence of serum antibodies in the Lyme patients studied. Or it may mean that serum was studied for the possible presence of a contaminating virus such as one that notoriously led to HIV/AIDS infections in hemophiliacs who used blood clotting agents during the 1960-1970s. Is “Lyme” disease caused by a contaminant in vaccines that is reactivated? Is it caused by a contaminant in insecticides which causes the intracellular infections to be released in the ticks and insects which feed upon us? You be the judge, but again I defer to my 2 most recent books to analyze this postulation.

A 1968 study of rabbit cry-immunology discusses immunoglobulin (antibody) production during the immune system’s antibody response to infection. The paper details that material injected into rabbits came from bacteria, viruses, or from other animal species. In all cases the experiments caused the production of heteroantibodies and not autoantibodies. This is important in the context of what Dr. Steere would hypothesize was the “cause” of so-called “chronic” Lyme disease. The studies led to the identification of specific antibodies that were produced by the rabbits’ bodies to the injected stimuli.

Is it possible that the presence of heteroantibodies, which are antibodies to foreign proteins, can be mistaken as “autoantibodies” in patients who have infections? Furthermore, I wonder whether heteroantibodies are sometimes made in response to reactivated vaccine virus proteins. This would describe proteins that are foreign (heterologous) in origin, but native (homologous) once incorporated into the human genome of the cell.

Can the insistence by Dr. Steere and his colleagues that persistent Lyme disease is an “autoimmune” disorder be the result of a misinterpretation of what the “autoimmune” antibody factors actually represent? Are “autoimmune” diseases really a proper immune reaction to foreign proteins?

Let’s take a look at a patent for a Lyme vaccine:

“Since the spirochete apparently contains multiple antigens capable of eliciting an immune response, the question arises from the prior art research as to why the anti-spirochetal immune response fails to clear the organism from the body. No answer is presently clear.”

In the later stages of disease, antibodies are sometimes made and these are used by lab tests to detect Bb. But in early stages, the spirochetes avoid detection by our immune system, and this is emphasized in many patents:

“Because the spirochete is so unabundant that it avoids detection by direct methods in infected patients, the humoral immune response of patients is used diagnostically to detect infection. The disease course as revealed by specific changes in immune response may be important in disease progression.”

“The immune response in the early stage disease is characterized by infiltration of the ECM lesion by macrophage and neutrophils (PMN). PBL derived T cells are unresponsive to spirochetal antigens and serum does not contain circulating antibodies. Activity of Natural Killer (NK) cells in both the early and late stage Lyme Disease patients is inhibited but NK function is normal in patients that are in remission. Analysis in vitro has shown that NK cells are actually inhibited by spirochetes. There is a characteristic B-cell hyperactivity displayed by patients in various stages of Lyme Disease.”

Spiroplasmas have spiralin proteins, which not incidentally, can, like Bb, cause this same kind of a B-cell response. This is all very interesting because in 1975 and 1977, soon after the public announcement of a “Lyme arthritis” outbreak in Connecticut, the National Institutes of Allergies and Infectious Diseases (NIAID) branch of the federal government awarded two research grants to Dr. L.P. Brinton, co-author of nearly a dozen articles from 1970-1975 with colleagues including Dr. Willy Burgdorfer. Dr. Brinton’s studies under these grants included Colorado tick fever virus development in Rocky Mountain wood ticks (Dermacentor andersoni), and the structure of the gut from normal and Rocky Mt. spotted fever (Rickettsia rickettsii)-infected ticks of the species.

The two grants also funded comparative work on the fine structure of wolbachia-like intracellular infections in various tick species; the structure of R. rickettsii and rickettsia species in brown dog ticks (Rhipicephalus sanguineus) from Mississippi; and the investigation of the spiroplasma 277-F agent from cotton tail rabbit ticks (Haemaphysalis leporispalustris).

If tick-carried spiroplasmas have absolutely nothing to do with Lyme disease, then it is entirely curious that “everybody” was so fascinated with them at the time of the Connecticut outbreak, including colleagues of Dr. Willy Burgdorfer (after whom the Bb agent would eventually be named). It is also rather curious that nothing whatsoever was stated about spiroplasmas when the causative agent of Lyme disease was announced in 1982, or audibly any time thereafter for that matter, over many decades whenever discussing the topic of Lyme disease.

Another factor to consider as a clue to “persistent” Lyme disease infections, is what the organisms do to the blood. In the case of our topic Rouleaux, we find that the aforementioned Waldenström’s disease, also called Waldenström’s macroglobulinemia or “WM”, is a B-cell cancer. B cells are a kind of white blood cell. The main antibody that is attributed to this problem is the Immunoglobulin M or IgM. Many people are familiar with Western blot tests for Lyme disease which detect IgM and IgG (Immunoglobulin G) antibody responses.

WM is a kind of lymphoma that is very slow growing, and is along the lines of an extremely low-grade non-Hodgkin’s lymphoma. The prevalence of this disorder in the general population is said to be very rare, with only about 1500 cases diagnosed in the US each year. However the disorder was discovered by a Swedish oncologist named Jan G. Waldenström in 1944, shortly after the introduction of the pesticide DDT. This may be a curious coincidence, or it may be an indication that pesticides have actually contributed to the rise of various cancers, including WM and/or the so-called “Lyme disease.”

How about them pesticide-laden “apples.” I bet you have never heard that hypothesis before.

Could WM be the same thing as “Lyme disease”? Well according to sources, maybe, maybe not. WM symptoms include the decrease of fibrinogen in the blood, which is a necessary component of making blood clots. But WM patients also suffer from a list of symptoms that sound vaguely Lyme-like. These include swollen lymph nodes (lymphadenopathy), increased viscosity (thick) blood from increased macroglobulin proteins (cryoglobulinemia), weight loss, fatigue, and chronic bleeding gums and/or nasal tissues. Also included on the symptoms menu are blurred or loss of vision, headaches, peripheral neuropathy (nerve pains and sensory problems), splenomegaly, or hepatomegaly (enlargement of spleen or liver). On occasion, stroke or coma occur, and a so-called “autoimmune” disease state. About 1/5 of the patients have this “thick” or sticky blood condition.

It is interesting that nearly half of WM patients have a particular kind of protein in their urine, called Bence Jones proteinuria. There is no cure for WM but patients can fall into a remissive state, and the disease is rarely but nevertheless, sometimes fatal. Corticosteroids and chemotherapeutic drugs are treatments of choice, and plasmapheresis can treat the hyperviscosity but does not cure the underlying cause. According to research, there are chromosomal abnormalities in the disorder, which include deletions of specific genes and overexpression by others. Gene therapies using stem cells have proven useful in some cases.

Isn’t this interesting that stem cell therapy has been attempted by some Lyme patients with mixed results?

Another interesting point to make is this:

There are external factors which have been implicated in causing WM disease. Those factors include the following:

  • exposure to farming
  • pesticides
  • wood dust
  • organic solvents

Genetic damage anyone? This brings us back to the two most recent books of mine, God Science, and The Fourth Monkey. In these ground-breaking books, I discuss quite intimately the “alleged” relationships between Lyme disease and how-do-you-like-this, each of these factors, with an emphasis on recombinant pesticides that are used industrially and agriculturally.

And I also quite “coincidentally” go into the description of the Lyme disease Bb agents and their specific relationships to each of these factors.

Whether Lyme disease is really another disease that causes a slow-growing B-cell cancer or not, may depend upon who is reading the research. From my perspective at least, the so-called “Lyme” disease is not only very different than how it has been described to be over decades; it is also very likely brought to you by the use of carefully formulated recombinant insecticides (this is genetic engineering folks), and the exposure of arthropods (ticks, mites) and insects to these tools. But then again if you follow the timelines outlined in my books, all of this will make a whole lot more sense.

And in the end, whether we are exposed to the Lyme disease organism in the first place, depends upon where we live, where we play, and what we do to protect ourselves. In the end, it may simply be attributable to a roll of the dice.

Or should I say, “rouleaux”?

1.) Bové JM, Mouches C, Carle-Junca P. et al. Spiroplasmas of Group I: The Spiroplasma citri Cluster. Yale J Biol Med. 1983;56 :573 -582 .
2.) Murray Polly. The Widening Circle. A Lyme Disease Pioneer Tells Her Story. 1996. St. Martin’s Press, NY.
3.) Tully JG, Whitcomb RF, Bové JM et al. Plant mycoplasmas: serological relation between agents associated with citrus stubborn and corn stunt diseases. Science 1973 ;182 :827 -829 .
4.) Clark HF, Rorke LB. Spiroplasmas of tick origin and their pathogenicity. In The Mycoplasmas, Volume 3. Plant and Insect Mycoplasmas. Whitcomb RF, Tully JG (ed.) New York, Academic Press. 1979:155-174.
5.) Zeigel RF, Clark HF. Electron microscopy of the suckling mouse cataract agent, a noncultivable animal pathogen possibly related to mycoplasma. Infect Immun. 1974 ;9:430-443 .
6.) Junca P, Saillard C, Tully JG et al. Caractérisation de spirooplasmes isolés d’insectes et de fleurs de France continentale, de Course et du Maroc. Proposition pour une classification des spiroplasmes. CR Acad Sci (Paris) 1980;Ser D 290:1209-1212.
7.) Whitcomb Robert F. The Biology of Spiroplasmas. Ann Rev Entomol. 198 1;26 :397 -425 .
8.) Clark HF. Suckling mouse cataract agent. J Infect Dis. 1964 ;114:476 -487 .
9.) Tully Joseph G, Rose David L, Yunker Conrad E, et al. Helical Mycoplasmas (Spiroplasmas) from Ixodes Ticks. Science 1981; 212(4498 ):1043 -1045 .
10.) Tully JG, Whitcomb RF, Rose DL, et al. Yale 1983 : Three serologically distinct groups of spiroplasmas have been recovered from ticks. Yale J Biol Med. 1983 Sept-Dec;603. [abstract]
11.) Tully JG, Whitcomb RF, Rose DL, et al. Characterization and Taxonomic Status of Tick Spiroplasmas: A Review. The Yale J Biol. Med. 1983 ;56 :599 -603.
12.) Megraud F, Gamon LB, McGarrity GJ. Characterization of Spiroplasma mirum (Suckling Mouse Cataract Agent) in a Rabbit Lens Cell Culture. Infect Immun. 1983 Dec;42 (3):1168 -1175 .
13.) Tully JG, Rose DL, Yunker CE, et al. Spiroplasma ixodetis sp. nov., a New Species from Ixodes pacificus Ticks Collected in Oregon. Inter J System Bacteriol. 1995 Jan;45 (1):23 -28 .
14.) Tenckhoff B, Kölmel HW, Wolf V, Lange R. Production and characterization of a polyclonal antiserum against Spiroplasma mirum (ATCC 29335 ). Zentralbl Bakteriol. 1994 Jan;28 0(3):409-415.
15.) Stanek G, Laber G, Hirschl A. Survival of spiroplasma on different carriers and resistance against three disinfectants. Proceedings of the 3rd International Organ. Mycoplasm. Custer, South Dakota, 1980 Sept. Abstract 107.
16. Tully JG, Rose DL, Yunker CE, et al. Spiroplasma ixodetis sp. nov., a New Species from Ixodes pacificus Ticks Collected in Oregon. Inter J System Bacteriol. 1995 Jan;45 (1):23 -28 .
17.) Williamson DL, Whitcomb RF, Tully JG, et al. Revised group classification of the genus Spiroplasma. Inter J Bacteriol. 1998; 48:1-12.
18.) Steere Allen C, Broderick Thomas F, Malawista Stephen E. Erythema Chronicum Migrans and Lyme Arthritis: Epidemiologic Evidence for a Tick Vector. Am J Epidemiol. 1978 ;108(4):312-32 1.
19.) Reik Louis, Steere Allen C, Bartenhagen Nicholas H, Shope Robert E, Malawista Stephen E. Neurologic Abnormalities of Lyme Disease. Medicine. 1979 ;58 (4):28 1-294 .
20.) Steere AC, Hardin JA, Malawista SE. Lyme arthritis: serum cryoprecipitates associated with skin and joint lesion. Arthritis Rheum. 1977 ;20:136 .
21.) Steere AC, Hardin JA, Malawista SE. Erythema chronicum migtans and Lyme arthritis: serum cryoimmunoglobulins and clinical activity of skin and joints. Science 1977;196 :1121-1122 .
22.) Shulman S, Witebsky E. The thyroid gland as source and target in autosensitization. Ann NY Acad Sci. 196 0;86 :400.
23.) US Patent 5,582,829. Alliger, et al. Sonicated borrelia burgdorferi vaccine. Filed July 28, 1992, published 12/10/1969. Assignee: Rx Technologies, Inc. (Garden City, NY).
24.) Shulman S, Bronson P, Clelia Riera, Brandt Eva J, Yantorno C. Studies in Cryo-Immunology. III. The Immunoglobulin Nature of the Antibody Response. Immunol. 1968 ;14:54 1-55 1.
25.) Sugarman Michael, Stobie Dennis G, Quismorio Francisco P, Terry Roger, Hanson Virgil. Plant Thorn Synovitis. Arthritis & Rheumat. 2005 Nov 2222;20(5):112525-112828.
26.) Johnston YE, Duray PH, Steere AC, Kashgarian M, Buza J, Malawista SE, Askenase PW. Lyme arthritis. Spirochetes found in synovial microangiopathic lesions. Am J Pathol. 1985985985 Jan;118(1):2626-3434.
27.) Gérard HC, Wang Z, Wang GF, et al. Chromosomal DNA From a Variety of Bacterial Species Is Present in Synovial Tissue From Patients With Various Forms of Arthritis. Arthrit Rheum. 2001 Jul;4444(7):1689-1697.
28.) Gran JT, Hjetland R, Andraessen AH. Pneumonia, myocarditis, and reactive arthritis due to Chlamydia pneumonia. Scand J Rheumatol. 1993 ;22 :43-44.


4 thoughts on “Lyme Rouleaux: Covert symptom or clue to something more?

  1. how do you treat rouleaux. I have air hunger sore legs; back; feet and even my hands are cold and feel a bit numb. Would this be the rouleaux.

  2. @kEITH, rouleaux has many causes. Sometimes it is simply dehydration. Other times infections and other issues. Best to talk with a qualified medical professional. I am not a doctor. Best.

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