Blowing the Whistle at the FDA, Jan 2001, exposing Dearborn and how OspA causes immunosuppression rather than, "was a vaccine."

01 Oct 2017


File List, RICO

1988 Steere says Lyme is like a B cell leukemia

Assoc Blogs-n-Webs:




Fungal Exosomes Inhibit Apoptosis

IDSA: "Vaccines serve the mfgs, not their victims"


BlumenthalAntiTrust Lawsuit

Exosomes, Blebs


CDC Admits Fraud, 2016
Dattwyler, 1988
Golightly, 1988
Dressler, 1994
BarbourFish, 1993
Dearborn, 1994

Pathogenic Fungi

Bush's warcrimes, Oct 2000




The 1989 IDSA's Journal, "Reviews of Infectious Diseases" Special Supplement 6, September-October, on Lyme and Spirochetal Diseases.

On this page is some of the data the Lyme crooks (Yale/ NYMC/ ALDF/ IDSA/ Kaiser cabal) refused to turn over to the Connecticut Attorney General for a year and a half before settling out of court.

This chapter is to include what was known about "Lyme Disease" up until the establishment of the RICO gang at New York Medical College in 1990 with Kaiser-Permanente.  The subsequent chapter on Biomarkers is meant to flesh out the truth about the seriousness of Lyme disease and OspA vaccination as both reported  but suppressed by this Lyme Mafia and how that negatively affected people with other very serious diseases.

1989 IDSA REVIEWS, FILE LIST: (neurologic disease Imitator, primarily) (Discusses treatment failure and neonatal Lyme) ("Epstein-Barr-like transformed B cells") (reversion from spheroplast takes months and not weeks; see Klempner's "bogus article") (treatment fails in half the cases, says Sigal, Steere, Dattwyler and Luft) (treatment endpoint unknown) (these neurologic diseases do not test CDC Dearborn-positive) (CDC officer Schmid says Lyme like other spirochetal diseases; treatment unknown)  Lyme and Lupus, by Allen Steere, and the reason Yale owned a Lyme and Lupus Clinic, now called L2-Diagnostics.
EARLY_CNS_INVASION.htm Benach - spirochetes invade the brain right away.
Dattwyler_Luft_Bb_DNA_in_CSF.htm  1994 FDA Meeting, Dattwyler and Luft talking about early CNS invasion of spirochetes, and then of course, they're permanent.

Dattwyler saying Bb invades the brain early:
LINK to PubMed, All, IDSA's 1989 "Special Supplement on Lyme" (47% association between ALS and Borreliosis, says JJ Halperin; these cases will not test Dearborn-positive, which is a homicide charge)
http://www.actionlyme,org/BARBOUR_MUTANTS_1992.htm  (antibodies exert "selection pressure," or all the Osps mutate, or, "Lyme is actually Relapsing Fever" and therefore vaccines won't prevent it.) (4 reports by Steere and Yale), 1992, Cold Spring Harbor ("Epstein-Barr-like transformed Chronic Lyme white blood cells")  ," by Allen Steere

RICO chronology, CDC instructs how to weaponize your Borrelia, 1964



←This disease described by JJ Halperin - now known as "fibromyalgia" which is officially, catastrophizing - is not detectable via the Dearborn/Steere method.

Neurologic abnormalities, seen in 11% of the cases (7) while ECM is still present or 1 to 6 months later, include aseptic meningitis [not detected by Mark Klempner in his 4.7 million dollar Femzalgia study, since he looked for extra white blood cells in the spinal fluid of his victims, of course knowing full-well what he was doing, criminally] encephalitis [now denied completely by Mark Klempner], choria, cerebellar ataxia, cranial neuritis, motor and sensory radiculitis, mononeuritic multiplex, the Guillain-Barre syndrome, and myelitis (2,8).  Encephalitis is usually mild, with somnolence, emotional liability, depression, impaired memory and concentration, and behavioral changes accompanied by EEG abnormalities.  Recovery may be incomplete (2).

"Lyme borreliosis-associated encephalopathy"--  JJ Halperin




LINK TO MEDLINE, ALL, "REVIEWS OF INFECTIOUS DISEASES," (the former name of the IDSA journal)  1989 Supplement; The status summary that lead to the creation of the cabal at New York Medical College and Kaiser-Permanente's takeover of "Lyme Disease"



Title page



Now we're really going to see some self-ass-biting.




1989 came after 1988, which was the Year of Lyme as a cause of Lower Motor Neuron Disease (ALS-like) and the Year of the Congenital Lyme Autopsy by Yale University and others, including Paul Duray, perhaps the world's top pathologist.  Paul Duray happens to be on the side of truth, which is Camp C, which is us, ActionLyme, the Greater Hartford Lyme Group, and the team.  Paul Duray works for everybody. He works for the National Cancer Institute.  He works for the Army, Ft. Detrick.

Scared yet?  You better be, because the National Cancer Institute is sort of in Ft. Detrick.  Ya wanna be more scared?  Duray worked with the famous Steven Hatfill - anthrax-mailer false-accusee - with NASA rotating tissue bioreactors (centrifugal force recreates gravity in zero-gravity) and guess what they found?

Spirochetes grow "exponentially" in human brain tissue in that NASA bioreactor bath.

Not only do viruses cause cancer and hang out with the US Army at Ft. Detrick, and not only are spirochetes more than happy to be doubly-rotating in human brain cells, but Paul Duray discovered that, "Hmmm.  These chronic Lyme victims' lymphocytes look like Epstein-Barr virus transformed or mutated cells."

Epstein-Barr transformed cells are quite interesting because these researchers like to use them due to the effect of Epstein-Barr on IMMORTALIZING cells.  That is, cells infected with Epstein-Barr somehow don't commit suicide upon the usual cues that non-EB infected cells do. 

[The non-committal of suicide by infected cells is a problem for chronic Lyme and LYMErix Disease®.  The disease itself, LYMErix Disease, I am trademarking since I am the one who organized the national campaign to get adverse events victims reported to the FDA, and then I explained exactly what happened with the LYMErix fraud, in scientific terms, to the FDA Vaccine Committee in January '01.  I think I will also be trademarking, um, Plum Island Slyme Disease® as that will refer to all the stealth disablers that harbor immune suppressing antigens.]

"Does Bb reactivate latent virus infections in tissues?"

Should we follow up on that?

Chugging along under this country's huge burden of neglect and abuse, crime, and dereliction of duty, I, myself tabulated the perfectly logical five years ago, but naturally no one understood it, adopted it, used it, came up with it logically on their own, nor do I think they understand it still:

What are the known syndromes associated with Lyme and what are the markers of them found out of range?

Then you create your laboratory around the tests you know need to be run.
And the Biomarkers contain the methods for how to detect the out-of-range markers.


Some of the BioMarkers found in Lyme are Matrix-metalloproteinases in the spinal fluid, glial fibrillary acidic protein in the spinal fluid (degradation of glial cells, or the energy-producing cells in the brain), QEEG abnormalities, autoantibodies, dysregulated interleukens (cytokines) in the blood, anti-heat shock proteins are hypothetically involved in neuroborreliosis, dysregulated monoamines (misuse of precursors to neurotransmitters, dysregulated neurotransmitters due to cytokines etc acting as neurotransmitters), anti-flagellin antibodies (Alan Barbour stated in a patent that this was the reason 41-kD or flagellin should not be used as a vaccine- they think anti-41 antibodies attach to neurons), blood-brain barrier abnormalities (decreased perfusion or blood flow to the brain, as demonstrated in SPECT imaging), abnormal PET scan or brain metabolism deficits, which may be the most significant marker patients need to end the harassment.



Glial Fibrillary Acid Protein X X ND ND X X X ND
Matrix-Metalloproteinase X X ND X X X X ND
Quinolinic Acid X X ND ND X X ND ND
T Cells StEeRe Diff/Dx? X X n/a X X X
CSF T Cells X given ? ND X X X ND
Antisulfatides ND X ND ND X X ND ND
Antigangliosides X X ND ND X X X ND
Pterins X X X X X X X ND
Anti-Heat Shock X X X ND X X X ND
SPECT X X            
EEG X X            
Antiphospholipids yes         obviously    
IL-6         X      
Haplotypes same for MS       X same for MS X ND



And, working with them (Kaiser literally is based, still, at New York Medical College in Valhalla, NY), just like the oil bankers thought they know what's best for America (fake wars and fake terrorists who happen to live right near the oil and nevermind the tearrists in East Timor or Rwanda or any other place we have to watch some punk-ass Pol Pot-wannabe play machete-king of the jungle with their rape-crusaders leaving in their wake the terms of endearment for the next generation's do-over), Kaiser-Permanente thinks they know what's best for America.  And just like the messy non-result we got in Iraq and Afghanistan and the resultant no allies, and Russia saying "things are worse now than they were during the Cold War" (Russian Federation Foreign Minister Sergei Lavrov, June 20, 2008), these idiots got a lawsuit and an international reputation for being "STUPID and INCOHERENT," in addition to being passed over for one billion dollars in research grants, just because everyone finally has had enough of their outrageous "LYMErix is the first ever placebo vaccine for Yuppie fake diseases" claims and want some real answers now.

These are not to mention how far and wide Lyme has spread because they lied about the vaccines and did not tell us that "RELAPSING FEVER means NO VACCINES ARE EVEN POSSIBLE."

We sufferers of this disease could hardly argue that that wasn't the worst result, despite for years not being believed even by those close to us and wishing this disease on those non-believers as the best medicine for such arrogant pukes.

No one can undo it.  It's permanent.  It's a Trojan Horse for those who think they're better now.

So, what is not clear?  How do we start to unscramble this nonsense?

The IDSA Reviews gave us lots of data on, well, the relatedness between the most prominent spirochetal diseases in America, anyway, Syphilis and Borreliosis.  They told us that re-culturing spirochetes could take months and not weeks in BSK media.  They told us that Lyme damages the brain and nerves directly.  They told us the treatment failed in half the cases and that the treatment endpoint was yet unknown.  And they told us we'd better WORRY about congenital Lyme.

They told us what we already knew because we HAVE this disease and we know how serious it is. 

Borreliosis is worse than Syphilis times two.



FROM the 1989 IDSA REVIEWS, Special Supplement on Lyme and spirochetal diseases:

RUSSELL JOHNSON, CULTURING   - Says Russell Johnson, spheroplasts could take months to revert to intact spirochetes in BSK media.  Have the crooks done this is recent history (KLEMPNER)??  Of course not.  Facts and truth were never part of the ALDF (Kaiser and the Patenteers) equation.

What do they look like in the meanwhile?

Hooo-boy, that's something you really have to look around for to see with your own eyeballs:
(PLUM ISLAND SLYME, humorously discussed by the Russian scientists associated with New York Medical College, somehow).

Willy Burgdorfer on spheroplasts/spheroblasts

And from one of the real pukes of medicine, Jorge Benach (who will really regret his comment that we Lyme victims are stupid, but that "Allen Steere has the science on his side," in a Letter to the Editor of the New York Times).





The causative agent of Lyme disease, Borrelia burgdorferi, is a highly neurotropic organism that not only can produce symptomatic neurologic disease but also can exist dormant within the central nervous system (CNS) for long periods. Two distinct types of neuroborreliosis occur at different stages of Lyme disease. Second-stage Lyme meningitis resembles aseptic meningitis and is often associated with facial palsies, peripheral nerve involvement, and/or radiculopathies. Lyme meningitis may be the first evidence of Lyme disease, occurring without a history of erythema chronicum migrans or flu-like illness. Third-stage parenchymal involvement causes a multitude of nonspecific CNS manifestations that can be confused with conditions such as multiple sclerosis, brain tumor, and psychiatric derangements. Manifestations of CNS parenchymal involvement in Lyme disease are generally associated, however, with a history of erythema chronicum migrans, meningitis, or carditis. Both second- and third-stage Lyme neuroborrelioses are commonly misdiagnosed because they are relatively uncommon and because they mimic many better-known disorders.



The multisystem effects caused by Borrelia burgdorferi in Lyme disease are multiple, varied, and unpredictable. In some patients, the full extent of the infection consists of a stage I acute systemic viral-like illness. Stage II primarily involves the cardiovascular system (myocarditis) and/or the central nervous system (CNS) (meningoencephalitis, polyradiculitis). More inflammatory cells are found in the heart and nervous system structures during this intermediate stage than are found in any tissues involved during stage I. Stage III is characterized by peripheral neuropathy and CNS disorders such as dementia or transverse myelitis and arthritis and synovitis of large joints such as the knee. Chronic Lyme disease is also associated with multiple and seemingly unrelated cutaneous manifestations such as acrodermatitis chronica atrophicans, sclerodermoid-like reactions, lichen sclerosus et atrophicus, subcuticular fibrous nodules, eosinophilic fasciitis-like lesions of the extremities, and, possibly, granuloma annulare. With care, spirochetes can be recovered or demonstrated by silver staining in most of the above lesions. Spirochetes have yet to be seen in the tissues of autonomic ganglia or peripheral nerves.

But by 2000, the monkey autopsies had been performed (this entire website was given in full-text hard-copy to James Phillips, a Yale perjuring malpractitioning sex-pervert):

"Nerve changes.  A detailed survey of the central nervous system lesions was carried out, which included 50 sampling sites.  The lesions observed are listed in Table 4.  Sensory ganglia of the dorsal root and trigeminal ganglia of animals J 831 and K 216 had individual neurons that immunostained positive with anti-Bb 7.5kD lipoprotein mAb (fig 16).  These neurons were swollen and were undergoing chromatolysis.  The dorsal root ganglia of the thoracic and cervical regions were especially affected.  Nerve sheath fibrosis within the spinal cord was limited to the thoracic segment in animal J 831.  Positive staining with anti-Bb mAb, accompanied by vacuolization of peripheral nerves, was observed in three of four animals. This change occurred as a radiculoneuropathy of the thoracic segment and peripheral nerves (Fig 17).  Animal L 131 had five peripheral nerves affected.  When the same nerves were stained for fat, focal vacuolization was observed (Figs 18 and 19). Focal demyelination  of the cervical cord was limited to J 831.  Lymphocyte infiltration of the affected nerves was mild in extent and confined to perivascular spaces. In animals L 131 and K 383, Bb could be demonstrated by immunostaining (Fig 20).

"  The pathogenesis of Lyme disease neuropathies is poorly understood...Sensory ganglia involvement has previously been described in human borreliosis (27-28). In our study, many of the ganglia positive for Bb by immunstaining were undergoing necrosis.  This staining was seen in two out of five animals and was not accompanied by a cellular infiltrate.

" Nerve tissues with perivascular lymphocyte infiltrate were present in three out of five animals.  This was the only lesions where extracellular Bb could be demonstrated. Peripheral cutaneous nerves were prominantly affected in the early phase of borreliosis of rhesus macaques(20, 28-29). Changes of the nervous system include the full range of changes observed in neuroborreliosis, which suggests a variety of disease mechanisms, including sensitization or mimicry as suggested by the vacuolization of peripheral nerves and cytokine-mediated destruction of nerves as a result of the infiltrating lymphocytes..."


The point of giving MDs scientific medical data would be for them to read it and learn about it.  It is not meant to be toilet paper or fodder for the diagnosis of "Unibomber Chemist," or "dangerously intelligent."  It is meant to be read and acquired as knowledge for the intrinsic value of knowledge itself- which is protection of oneself and others from FRAUD or a lie.




Objective measures of neurologic function were used to assess response to treatment in patients with late Lyme borreliosis. Neurophysiologic evidence of peripheral neuropathy was present in 64 of 137 patients tested. Measures of distal axon function (sensory amplitude and conduction velocity, motor terminal latency) were most affected. Repeat studies following 60 patients receiving antimicrobial therapy demonstrated significant improvement in these values. Before and after therapy 17 patients with late Lyme borreliosis and prominent subjective cognitive dysfunction underwent neuropsychologic tests of memory, conceptual ability, concentration, psychomotor function, overlearned intellectual abilities, and mood. Significant abnormalities were evident before treatment; all reversed with antimicrobial therapy. Many patients with this encephalopathy had specific abnormalities revealed by magnetic resonance imaging of the brain and had evidence of intrathecal synthesis of antibody to Borrelia. These findings indicate that late Lyme borreliosis commonly causes nervous system abnormalities that are reversible with appropriate antibiotic therapy.


As we now know (more recently from Brian Fallon at Columbia and I know, myself, from personal experience) these patients tend to relapse, but more importantly, Mark Klempner reported that there is no such thing as cognitive compromise in Lyme victims.

You can get psychiatrists to say anything, as previously mentioned:

Cognitive function in post-treatment Lyme disease: do additional antibiotics help?

University of Connecticut School of Medicine, Farmington, USA.

BACKGROUND: It is controversial whether additional antibiotic treatment will improve cognitive function in patients with post-treatment chronic Lyme disease (PTCLD). OBJECTIVE: To determine whether antibiotic therapy improves cognitive function in two randomized double-blind placebo-controlled studies of patients with PTCLD. METHODS: A total of 129 patients with a physician-documented history of Lyme disease from three study sites in the northeast United States were studied. Seventy-eight were seropositive for IgG antibodies against Borrelia burgdorferi, and 51 were seronegative. Patients in each group were randomly assigned to receive IV ceftriaxone 2 g daily for 30 days followed by oral doxycycline 200 mg daily for 60 days or matching IV and oral placebos. Assessments were made at 90 and 180 days after treatment. Symptom severity was measured from the cognitive functioning, pain, and role functioning scales of the Medical Outcomes Study (MOS). Memory, attention, and executive functioning were assessed using objective tests. Mood was assessed using the Beck Depression Inventory and Minnesota Multiphasic Personality Inventory. RESULTS: There were no significant baseline differences between seropositive and seronegative groups. Both groups reported a high frequency of MOS symptoms, depression, and somatic complaints but had normal baseline neuropsychological test scores. The combined groups showed significant decreases in MOS symptoms, higher objective test scores, and improved mood between baseline and 90 days. However, there were no significant differences between those receiving antibiotics and placebo. CONCLUSION: Patients with post-treatment chronic Lyme disease who have symptoms but show no evidence of persisting Borrelia infection do not show objective evidence of cognitive impairment. Additional antibiotic therapy was not more beneficial than administering placebo.


So, there you have it.  "Lyme is an imaginary disease prevented by the placebo vaccine, LYMErix," says Mark Klempner, now the head of a CDC bioweapons level IV lab in Boston.


DATTWYLER and LUFT, "Treatment fails in half the cases and we better be worried about pregnant women with Lyme."



Immune responses to Borrelia burgdorferi infection are now well characterized. Following infection there is an early T cell response and a more slowly evolving B cell response. IgM antibodies appear first and are followed by IgG and IgA. Early antibodies are primarily against a 41-kilodalton flagellum-associated antigen; responses to other spirochetal antigens develop later. Serologic assays that use whole B. burgdorferi preparations are not always able to detect an early rise in antibodies above a background of crossreactive antibodies present in most uninfected individuals. Moreover, some individuals with neurologic involvement who lack diagnostic levels of serum antibody to B. burgdorferi have high levels of the antibody in their cerebrospinal fluid. Specific T cell blastogenesis [used by Allen Steere to diagnose inhaled spirochetes in his lab workers] to B. burgdorferi can further document infection. Analysis of T cell subsets in Lyme arthritis demonstrates a marked decrease in the CD4+2H4+ subpopulation in the synovial fluid, although normal numbers of these cells are present in peripheral blood. Immunologic measurements are useful in evaluating and treating a wide array of patients who may be infected with B. burgdorferi.


TMT of SYPHILIS, CEF RECOMMENDED, ENDPOINT UNKNOWN  "Recent evaluations of ceftriaxone for early syphilis therapy are promising; however, the optimal dose and duration of therapy are unknown."




RELATED and reported at around that time:

ALS and Lyme - by JJ Halperin and Ray Dattwyler, authors of the new and bogus IDSA Guidelines

"Of 19 unselected patients with the diagnosis of amyotrophic lateral sclerosis (ALS) living in Suffolk County, New York (an area of high Lyme disease prevalence), 9 had serologic evidence of exposure to Borrelia burgdorferi."

47%;   9 of 19 men with Lou Gehrig's Disease in a Lyme-endemic area were exposed to borrelia


Bb INFECTION OF THE BRAIN (plasmid changes)- PACHNER, 1990




Roland Martin's former NINDS-MS homepage (he went home to Germany)

Oligoclonal bands in the CFS of Lyme victims (and MS, again, by NINDS' former Roland Martin who went home to Germany because he did not prove Lyme is a cause of MS as an autoimmune T cells disease, just like Steere did not prove Lyme is an T cell autoimmune disease)  The usefulness of the Roland Martin reports is that they refute Steere's notion that Lyme is just a bad knee.

Roland Martin's Autoreactive BRAIN and NERVE T cells in the spinal fluid of Lyme Borreliosis.  This mechanism of pathology really has not been proven.  There does not seem to be any real T cell autoimmunity going on, here, in Lyme/MS, as least as a process researchers can re-create in a lab.




NEW, CDC says-- "Human infection by Borrelia burgdorferi, the etiological agent for Lyme disease, can result in serious acute and late-term disorders including neuroborreliosis, a degenerative condition of the peripheral and central nervous systems."  -  THIS KIND OF LYME IS UNDETECTABLE WITH CDC'S CURRENT TESTING STANDARD, AND THE CDC KNOWS IT.


Direct destruction of nerve and brain cells, Benach  by Jorge Benach, who sent a letter to the editor of the New York Times stating that Allen Steere was right, that no one had Lyme disease, and that the people who claimed that they did (that they did not have the imaginary Allen Steere in Europe kind of imaginary self-limiting autoimmune knees disease), were crazy, and  that Steere was right and "has the science on his side," when Steere had said that we don't have a chronic brain disease, but that we had "some psychiatric illness" when it would be some psychiatric illness for these lying Lyme crooks be lying their ugly faces off about us and about "Lyme Disease," and it is psychiatry who does not have science on their side:

J Infect Dis. 1990 Jun;161(6):1187-93.Links

Borrelia burgdorferi in the central nervous system: experimental and clinical evidence for early invasion.

Department of Pathology, State University of New York, Stony Brook 11794-8691.

Intravenous injection into adult Lewis rats of live Borrelia burgdorferi, the spirochetal agent of Lyme disease, was followed by increased permeability of the blood-brain barrier. Permeability was measured by the ratio of 125I-labeled albumin in cerebrospinal fluid to that in blood. Permeability changes were dose-dependent, began 12 h after inoculation, and reversed within 1 week. Only live, intravenously inoculated organisms produced impairment of the blood-brain barrier. A spirochetal strain-dependent effect was noted in that changes were more marked with a recent isolate than with a strain in long-term in vitro culture. Mild pleocytosis and spirochetes were noted in the cerebrospinal fluid of rats with increased blood-brain barrier permeability. This experimental evidence for early central nervous system invasion was pursued in studies of the human disease. Specific B. burgdorferi antigens could be detected in the cerebrospinal fluid of patients with early Lyme disease by use of murine monoclonal antibodies as probes.


And Stroke.

And Immune Complex-Vasculitis.
And rosetting.
And the tolerance to new fungal antigens that hijack oxygen transfer by modifying the osmotic potential.
And the activation of latent viruses-  CANCER

Happy with IDSA now?





LINK TO MEDLINE, ALL, "REVIEWS OF INFECTIOUS DISEASES," (the former name of the IDSA journal)  1989 Supplement; The status summary that lead to the creation of the cabal at New York Medical College and Kaiser-Permanente's takeover of "Lyme Disease"


Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1511-7.Links

Treatment of syphilis: current recommendations, alternatives, and continuing problems.

Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland.


Duray PH.
Clinical pathologic correlations of Lyme disease.
Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1487-93.
PMID: 2814170 [PubMed - indexed for MEDLINE]


  Berger BW.
Dermatologic manifestations of Lyme disease.
Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1475-81.
PMID: 2814169 [PubMed - indexed for MEDLINE]


[No authors listed]
Lyme disease and other spirochetal diseases. Proceedings of a symposium. Washington, D.C., 29 February-1 March 1988.
Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1433-525. No abstract available.
PMID: 2814168 [PubMed - indexed for MEDLINE]
Luft BJ, Gorevic PD, Halperin JJ, Volkman DJ, Dattwyler RJ.
A perspective on the treatment of Lyme borreliosis.
Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1518-25. Review.
PMID: 2682965 [PubMed - indexed for MEDLINE]

"The Treatment of Lyme Fails in Half the Cases" -- Ray Dattwyler, Ben Luft, Lenny Sigal and Allen Steere




Johnson RC.
Isolation techniques for spirochetes and their sensitivity to antibiotics in vitro and in vivo.
Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1505-10. Review.
PMID: 2682963 [PubMed - indexed for MEDLINE]

Culturing, Russell Johnson:  In this report he talks about the low recovery rate of spirochetes from culture, and that it in some cases it may take months for the spirochetes to revert from the spheroplast form.



Halperin JJ.

Abnormalities of the nervous system in Lyme disease: response to antimicrobial therapy.   Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1499-504. Review. Erratum in: Rev Infect Dis 1990 May-Jun;12(3):566.   PMID: 2682962 [PubMed - indexed for MEDLINE]



Dattwyler RJ, Volkman DJ, Luft BJ.
Immunologic aspects of Lyme borreliosis.
Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1494-8. Review.
PMID: 2682961 [PubMed - indexed for MEDLINE]


Pachner AR.
Neurologic manifestations of Lyme disease, the new "great imitator".
Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1482-6. Review.
PMID: 2682960 [PubMed - indexed for MEDLINE]


Barbour AG.
The molecular biology of Borrelia.
Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1470-4. Review.
PMID: 2682959 [PubMed - indexed for MEDLINE]


Schmid GP.
Epidemiology and clinical similarities of human spirochetal diseases- by the Centers for Disease Confabulations
Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1460-9. Review.
PMID: 2682958 [PubMed - indexed for MEDLINE]


Anderson JF.
Epizootiology of Borrelia in Ixodes tick vectors and reservoir hosts.
Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1451-9. Review.
PMID: 2682957 [PubMed - indexed for MEDLINE]


Burgdorfer W, Hayes SF, Corwin D.
Pathophysiology of the Lyme disease spirochete, Borrelia burgdorferi, in ixodid ticks.
Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1442-50. Review.
PMID: 2682956 [PubMed - indexed for MEDLINE]


Ciesielski CA, Markowitz LE, Horsley R, Hightower AW, Russell H, Broome CV.
Lyme disease surveillance in the United States, 1983-1986.
Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1435-41.
PMID: 2682955 [PubMed - indexed for MEDLINE]


Dammin GJ.
Erythema migrans: a chronicle.
Rev Infect Dis. 1989 Jan-Feb;11(1):142-51.
PMID: 2644687 [PubMed - indexed for MEDLINE]


"Chronic Neurologic Lyme Disease," by Allen Steere, who now calls disease this "CRAZY."









"The triad of neurological manifestations of Lyme disease," by Allen Steere and Andrew Pachner



Saint Michael the Archangel,
defend us in battle.
Be our protection against the wickedness and snares of the devil.
May God rebuke him, we humbly pray;
and do Thou, O Prince of the Heavenly Host -
by the Divine Power of God -
cast into hell, satan and all the evil spirits,
who roam throughout the world seeking the ruin of souls.