Mrs. Steere must be very proud this Mother’s Day. She’s probably dead, like my mom—except from old age, unlike my mom—who likely died from complications of late-stage untreated Lyme disease. But, hey—surely they’re looking over us both with their motherly approval.
Mrs. Steere’s boy Allen has really made a name for himself, having published hundreds of research articles, primarily on Lyme disease. She must be especially proud that he made something of his life after abruptly changing course in his last year of med school to learn about epidemiology to avoid the draft. What’s more, he published lots and lots of research that clearly went far beyond rheumatology, his area of specialization. One might be inclined to call him an over-achiever.
How rare for a doctor who specializes in old lady joint deterioration to be so passionate about a disabling, deadly, infectious disease. Nice of the State of Connecticut to recognize him for that.
“For this breakthrough work, Dr. Steere has been widely heralded. At a ceremony in Hartford last year (1998) Gov. John G. Rowland proclaimed Sept. 24 as Allen C. Steere Day.”
Congratulations, Mrs. Steere! What a fine man you raised. From draft dodger to disease detective, he really turned his life around, didn’t he?
I hope the children of Lyme-infected mothers have the same opportunities to make an impact upon society, given that there could be millions of them out there, suffering all kinds of random undiagnosed consequences. Goodness, they may not even have known about it, had Allen not published in 1988 that congenital transmission of Lyme disease is a real concern.
I’m sure there are hundreds of thousands—if not millions—of mothers out there who recognize the importance of this research to their families, as well. So, forgive me, Mrs. Steere, but this is the part where I point out that your boy never really lost his draft-dodger tendencies. He did, however, irretrievably lose his balls.
The basic timeline goes like this:
Allen joins the Epidemic Intelligence Service (EIS, a CDC division) right out of medical school “as a dodge” to avoid the draft and being sent overseas.
Allen “practiced the science of epidemiology across America.”
Allen begins “a fellowship at Yale in his passion, rheumatology. ‘I hoped that my C.D.C. experiences were something I could apply to the study of arthritis,’ he said.”
Allen is put back into service by the EIS to investigate a strange outbreak among children in Lyme, CT.
The Bayh-Dole Act began allowing universities and their researchers to profit off of intellectual property arising from federal government-funded research.
Throughout the 1980s
Allen publishes repeatedly about the ill effects of infection with B. burgdorferi that go far beyond an arthritic knee.
1983, for example:
The early clinical manifestations of Lyme disease.
“Lyme disease, caused by a tick-transmitted spirochete, typically begins with a unique skin lesion, erythema chronicum migrans. Of 314 patients with this skin lesion, almost half developed multiple annular secondary lesions; some patients had evanescent red blotches or circles, malar or urticarial rash, conjunctivitis, periorbital edema, or diffuse erythema. Skin manifestations were often accompanied by malaise and fatigue, headache, fever and chills, generalized achiness, and regional lymphadenopathy. In addition, patients sometimes had evidence of meningeal irritation, mild encephalopathy, migratory musculoskeletal pain, hepatitis, generalized lymphadenopathy and splenomegaly, sore throat, nonproductive cough, or testicular swelling. These signs and symptoms were typically intermittent and changing during a period of several weeks. The commonest nonspecific laboratory abnormalities were a high sedimentation rate, an elevated serum IgM level, or an increased aspartate transaminase level. Early Lyme disease can be diagnosed by its dermatologic manifestations, rapidly changing system involvement, and if necessary, by serologic testing.”
So, it was a multi-system disease that could be diagnosed clinically, and serologic testing wasn’t even necessary.
“The isolate from the cerebrospinal fluid was recovered in primary culture after two weeks of incubation; it was from a patient who had chronic meningitis. Two and a half months previously, ECM had developed in this patient and had been followed by intermittent headache, stifneck, fever, right-sided facial palsy, arthritis of the elbows, hips, and knees, malaise, and fatigue.”
THE YALE JOURNAL OF BIOLOGY AND MEDICINE 57(1984),453-461
The Clinical Spectrum and Treatment of Lyme Disease
“Regardless of the antibiotic agent given, nearly half of patients still experienced minor late complications– recurrent episodes of headache or pain in joints, tendons, bursae, or muscles, often accompanied by lethargy . Their physical examinations were usually normal. Symptoms were often reminiscent of those experienced at the beginning of the illness, but were generally briefer and less severe. They correlated significantly with the initial severity of the illness. In a given attack, pain usually occurred in one or two sites and lasted from hours to days. With frequent attacks, the pain was often migratory. Such attacks sometimes recurred for several years.”
Lyme disease was TERRIBLE and suspiciously close to CANCER, and racing across the country! Oh no! We needed a VACCINE! Thank GOD for 1986!
Allen’s report, “Antigens of Borrelia burgdorferi recognized during Lyme disease. Appearance of a new immunoglobulin M response and expansion of the immunoglobulin G response late in the illness,” becomes the basis for the diagnostic guidelines for almost the whole world! Band 41 on the Western blot will do it, as will varying bands over time,
“The National Childhood Vaccine Injury Act (NCVIA) of 1986 (42 U.S.C. §§ 300aa-1 to 300aa-34) was signed into law by President Ronald Reagan on Nov 14, 1986, in the United States, to reduce the potential financial liability of vaccine makers due to vaccine injury claims. The legislation was aimed at ensuring a stable market supply, and to provide cost-effective arbitration for vaccine injury claims. Under the NCVIA, the National Vaccine Injury Compensation Program (NVICP) was created to provide a federal no-fault system for compensating vaccine-related injuries or death by establishing a claim procedure involving the United States Court of Federal Claims and special masters.”
Hooray! That meant that they could use federal grant money to fund vaccine “research,” profit personally from all of the “inventions,” and then not face any liability when the fake vaccines actually caused the disease! Way to go, Mrs. Steere! Your boy’s running with the popular kids!
Allen publishes “Clinical Pathologic Correlations of Lyme Disease by Stage” with Paul Duray. In this report they describe numerous disabling manifestations of the disease that are eerily similar to cancer. This is the same report cited earlier, where he mentioned “resultant congenital infections and fetal demise”:
“Not only are plasma cells plentiful in the spleen, lymph nodes and bone marrow, they are also represented by large and somewhat atypical-appearing precursor B cells as well.”
“Numerous names have been given to this stage, including pseudolymphoma, lymphoid hyperplasia, follicular hyperplasia, lymphocy-toma cutis, Spiegler-Fendt lymphoid hyperplasia, and lymphadenosis benigna cutis of Baverstedt.”
“The immune response involves virtually all of the organs and structures of the reticuloendothelial system including the bone marrow, and clinical pain and discomfort seems to correlate with hyperplasia of lymph nodes and spleen and bone marrow. Diffuse visceral involvement in this acute stage mimics infectious mononucleosis or disseminated viral syndromes. These include conjuctivitis, pharyngitis, pneumonitis with dry cough and mild pleuritic pain, hepato-splenic tenderness, lymph node swelling of the neck and groin, and orchitis. There is lymphoid hyperplasia of the lymph nodes and spleen consisting of prominent germinal centers and numerous perifollicular lymphocytes, with proliferation of plasma cell precursors and mature plasma cells. *The plasma cell precursors are large, appear tumor-like, and can resemble Reed-Sternberg cells.”*
“The red pulp of the spleen is congested, not unlike that seen in infectious mononucleosis. Spirochetes can be demonstrated in the lymph nodes, spleen and bone marrow and liver. There is a transient hepatitis reflected by elevated liver cell enzymes such as SGOT, SGPT, and GGT. The liver can vary from a mild lymphocytic portal triaditis all the way to liver cell derangement that simulates acute viral hepatitis.”
“One hepatitis case from Wisconsin showed a remarkable number of mitoses of liver cells, itself a very unusual finding in non-neoplastic conditions of the liver.”
“Cardiovascular system involvement is manifested by one or more forms of cardiac arrhythmia. Patients may have either an incomplete (first or second degree) AV block or a complete AV block. Some patients appear not to be aware of their arrhythmias during this stage.“
If you get the picture, you could skip ahead here, right past the next block quote, unless you want to read about even more manifestations that any moron can see do not describe a simple ouchie knee.
“Clinical signs and symptoms of meningoencephalitis are fully developed in stage II. Patients have headache, photophobia, and signs of meningismus. This stage is paralleled by CSF pleocytosis. In terminal cases seen thus far, band-like infiltrates of lymphocytes and plasma cells are seen in the leptomeningeal layers. Some cases have shown mild spongioform changes of the cerebral cortex, and others have shown an increase in oligodendrocytes, which at times are situated in cuffs around small vessels. Microgliosis of a focal nature was seen in one young male in coma who responded to intravenous penicillin therapy (FIG.5). Spirochetes were demonstrated in that case. Patients have either severe encephalopathy including stupor and coma, or varied forms of psychoneurosis including depression. Many of these are also found in stage III disease. These encephalopathic stages may be entirely absent, and patients present with various combinations of cranial neuritis. Bilateral Bell’s palsy is a prominent feature in some stage II patients, and almost constitutes a firm clinical sign that a given patient in an endemic area with bilateral Bell’s palsy has Lyme disease until proven otherwise. Also the clinical triad of cranial neuritis, meningitis, and radiculoneuritis also constitutes Lyme disease in an endemic area unless proven otherwise. Aggregates and groups of lymphocytes are found infiltrating the autonomic ganglia directly as well as the afferent and efferent rootlets. Plasma cells are not so prominent as are the lymphocytes in this stage. We have
not seen spirochetes in the ganglia, but the assumption is that they are directly present.”
“We have had recent experience with a lesion that is not uncommonly seen in late stage II in Europe, and that consists of a lesion manifested clinically by extreme pain in one or more proximal muscle groups such as the musculature of the thigh or forearm. This pain is not that of the stage I myalgia but is one of pain at rest as well as in motion. Clinically there is swelling and tenderness of involved muscle groups. This lesion appears to be independent of peripheral neuropathy or central nervous system involvement, although they may coexist. Biopsy shows perivascular infiltrates of lymphocytes and plasma cells of vessels within the muscle itself.”
“The duration of Lyme myositis is not known, but it probably can persist for variably long periods.”
“Stage III (TABLE3) is the chronic phase of Lyme disease, usually beginning months after initial onset, and lasting into many years. Stage III is characterized by involvement of the joints (intermittent oligoarthritis), peripheral nervous system, skin and subcutaneous soft tissue.”
“In chronic and severe forms, there may be nerve fiber loss, demyelination, and changes not unlike that of Wallerian degeneration.”
“Two cases of lichen sclerosus (et atrophicus) have now been seen in chronic Lyme disease patients by us and by others.23 Both had the upper papillary dermal homogeni-zation of the collagen with an edematous appearance as seen in classic LSEA, and also had the band-like mid-dermal lymphocytic infiltration. Again in both of these cases, the deeper dermal vessels showed occlusive changes.”
“Lyme disease is capable of producing a wide variety of clinical pathologic conditions and lesions having in common histologic features of collagen-vascular disease. The plasma cell is an omnipotent inflammatory responder in most tissues involved by Lyme disease, ranging from relatively acute to lesions that have gone on for years. Vascular thickening also seems to be prominent, and in the dermis is accompa- nied by scleroderma-like collagen expansion. The disease in some ways resembles the responses seen in lupus erythematosus such as mild cerebritis with lymphocytes and plasma cells in the leptomeninges. Lymphoplasmacytic panniculitis of Lyme disease resembles lupus profundus, both in the infiltrate and the plasma cell-blood vessel relationship. The onion skin thickened vessels of the synovia resemble the vessels of lupus spleens, while the scleradermoid thickening of the dermis and various skin lesions of stage III Lyme disease suggest a collagen-vascular disorder. Finally, the perivascular lymphoid infiltrate in clinical myositis does not differ from that seen in polymyositis or dermatomyositis. All of these histologic derangements suggest immunologic damage in response to persistence of the spirochete, however few in number.”
Allen’s buddies establish the “enterprise,” the American Lyme Disease Foundation (ALDF), to act as the financial-backing and propaganda arm of the Vector-Borne Diseases Diagnostic & Prophylactic Racketeering Organization. From this point on, “May the odds be ever in your favor!” (Sorry, couldn’t resist.)
LYMErix Phase I trials were underway at this time.
Whaddaya know? Allen publishes about bad-knee Lyme being an HLA-linked outcome, thus setting the stage for his work with Frank Dressler that must have made mom really proud.
Don’t all moms simply glow over their children’s research fraud that causes millions of victims to suffer from a mystery illness that’s denied by all of medicine?
Allen falsifies Lyme disease testing: uses “high passage strains” and “OspA and B without the lipid attached” to leave OspA and B out of the standard for his later monopoly on vector borne diseases testing. Only Corixa, Imugen and Yale were to be licensed to use the RICO strain patent by Dave Persing (US Patent # 6,045,804)
J Infect Dis. 1994 Feb;169(2):313-8.
Antibody responses to the three genomic groups of Borrelia burgdorferi in European Lyme borreliosis. Dressler F1, Ackermann R, Steere AC.
Good job, Allen!
Yale patents LYMErix/OspA
1994 (Busy Year)
Allen’s “research” with Dressler forms the basis of the proposed *new* diagnostic standard at the CDC’s Dearborn conference. The Lyme disease case definition now means that only the HLA-linked bad-knee cases are counted. The other 85% of victims are now denied diagnosis and treatment, sent to psych, and slandered to death.
Lyme is no longer a multi-system disease that can be diagnosed clinically, without serologic testing. Now, you have to jump through 18 hoops while patting your head, rubbing your tummy, and repeating, “Lyme disease is only a knee. Lyme disease is only a knee. Lyme disease is only a knee.”
The Time Warp Since 1994, DEARBORN
Oh, Mrs. Steere, your boy is having trouble keeping his story straight! Like here, in a 2003 presentation at Harvard. Just kidding on that congenital transmission thing and fetal demise! LOLZ!
“What is the risk of maternal-fetal transmission of the spirochete?”
“Several provocative cases in the past have caused concern that maternal-fetal transmission of the spirochete may cause adverse outcomes in the fetus. However, subsequent prospective studies have not been able to identify a case in which the spirochete has been shown to cause fetal damage. In a study of pregnant white-footed mice, all of whom were infected with the spirochete, there was an absence of transplacental transmission of the spirochete to their offspring. Thus, maternal-fetal transmission of the spirochete would seem to occur rarely, if at all.”
Mrs. Steere, did you ever tell your draft-dodging boy that it’s not good to lie?
Ask ANY Lyme victim, and they can tell you how we’re sneered at by doctors, dismissed for being “noncompliant,” called crazy and hypochondriacal, and the worst—HYSTERICAL, which is a misogynistic term used to intimidate women into submission.
FACT: All of this medical abuse is a direct result of the lies spoken and published by the ALDF/CDC/Yale enterprise since the early 1990s. That’s right: 25 years of ABUSE heaped upon FAILURE TO TREAT a real, organic illness that Allen Steere said was similar to cancer, before he said it was just a bum knee.
This report pretty much sums it up:
Antiscience and ethical concerns associated with advocacy of Lyme disease.
Lancet Infect Dis. 2011.
Auwaerter PG1, Bakken JS, Dattwyler RJ, Dumler JS, Halperin JJ, McSweegan E, Nadelman RB, O’Connell S, Shapiro ED, Sood SK, Steere AC, Weinstein A, Wormser GP.
“Advocacy for Lyme disease has become an increasingly important part of an antiscience movement that denies both the viral cause of AIDS and the benefits of vaccines and that supports unproven (sometimes dangerous) alternative medical treatments. Some activists portray Lyme disease, a geographically limited tick-borne infection, as a disease that is insidious, ubiquitous, difficult to diagnose, and almost incurable; they also propose that the disease causes mainly non-specific symptoms that can be treated only with long-term antibiotics and other unorthodox and unvalidated treatments. Similar to other antiscience groups, these advocates have created a pseudoscientific and alternative selection of practitioners, research, and publications and have coordinated public protests, accused opponents of both corruption and conspiracy, and spurred legislative efforts to subvert evidence-based medicine and peer-reviewed science. The relations and actions of some activists, medical practitioners, and commercial bodies involved in Lyme disease advocacy pose a threat to public health.”
https://www.ncbi.nlm.nih.gov/m/pubmed/21867956/ (Check out the “similar articles” while you’re there!)
(Mrs. Steere, was Allen bullied as a child? Because he seems to have some aggression issues against vulnerable people.)
And, to truly ice the cake, the cabal knew very well–PRIOR TO the formation of the ALDF–that the disease is caused by the very lipids that went into making LYMErix.
Raymond Dattwyler, 1988, saying that the disease is attributable to the “supernatants,” or the oils, or lipids, from the Osps.
Ann N Y Acad Sci. 1988;539:103-11.
Modulation of natural killer cell activity by Borrelia burgdorferi.
Golightly M1, Thomas J, Volkman D, Dattwyler R.
“..when lymphocytes are cultured in the presence of growing Bb there is a marked inhibition ( p < .0005 ) of NK activity on days 3, 5, and 7 when compared to lymphocytes cultured in BSKII media in the absence of spirochetes. This effect is not due to a selective depletion or or toxicity to endogenous NK since viability studies and monoclonal antibodies demonstrate no significant changes after culture with the organism.”
“The inhibition is directly attributable to the organism or its supernatants (data not shown).”
Borrelial lipids cause immunosuppression, is what he is saying.
Here is what else Luft and Dattwyler said in IDSA’s journal in 1989 (so Allen is fully aware of it) about how treatment fails, and how this may be due to “pathological changes that occur prior to treatment” confirmed by Baumgarth when she showed infection with Borrelia damaged B cell germinal centers and rendered victims unable to deal with a common viral infection like influenza.
Rheum Dis Clin North Am. 1989 Nov;15(4):747-55. Treatment of Lyme borreliosis.
Luft BJ1, Dattwyler RJ. https://www.ncbi.nlm.nih.gov/pubmed/2555849
FAILURE RATES OF >50% ARE BEING REPORTED….CLEARLY, ALTERNATIVE THERAPIES ARE NEEDED. CLEARLY. NOT “YOU’RE NUTS; GO AWAY.” Because treatment fails half the time. Say Dattwyler & Luft, Allen Steere “Regardless of the antibiotic agent given, nearly half of patients still experienced minor late complications-recurrent episodes of headache or pain in joints, tendons, bursae, or muscles, often accompanied by lethargy .” (1983), and Charles Chiu (UCSF, 2016).
And NOW, guess what? Can you guess?
So, ultimately, what that means is that Allen and the crew again admit that Lyme might be a little worse than just a knee. Sound the alarms, blare the sirens: Lyme disease is a disease again, and we need a vaccine. Again.
“This finding suggests that there is redundancy in the ability of the innate immune system to recognize B. burgdorferi and/or that these components can activate pathways that produce anti-inflammatory cytokines, … – the anti-inflammatory effects might be the more important function of TLR signaling.”
“The anti-inflammatory effects might be the more important function of TLR signaling.” Ya think? You mean the immunosuppression? The sick people might be more important than the not sick people? Thats great. Yep. A “vaccine” is just what we need for a disease we already have, that isn’t really a disease, but wait….oh, yeah, it is, but we don’t know what OspA is….never mind that it caused the disease, itself.
Thank you, Mrs. Steere. Thank you for endowing the world with this gigantic piece of human excrement named Allen.
See the Occam’s Razor for more data on not-Lyme post-sepsis AIDS.