Illinois Shooter Maybe Crazy, But Not Because of Lyme Disease

Did you catch this story? A man in Illinois walks into a church and shoots the pastor. After killing the pastor, his gun jams, he grabs a knife and starts stabbing himself. At which point, he is tackled by two guys and remanded into custody.

Now his lawyer is claiming that his mental status was impaired because he had Lyme disease. (And, shocker: this interpretation of the story is being pushed over at Huffington Post.)

Listen, this guy may be crazy. In fact, he undoubtedly has severe emotional and neurological problems. But Lyme disease isn't why.

Lyme disease is caused by a bacteria, Borrelia burgdorferi transmitted to humans by the bite of deer ticks infected. It is endemic to the Northeast and Midwestern US. You are out raking leaves one day in the woods, and a tick that carries the bacteria bites you. If the tick carries the disease and you don't see the bite, the bacteria can travel through the blood and set up shop in your body causing the disease.

Early stages of Lyme disease show a very characteristic "bulls-eye" shaped rash called erythema migrans (pictures here). The rash is associated with joint pains, chills, fever, headache, and fatigue. Later the disease can cause neck stiffness, numbess or tingling in the extremities, and facial paralysis. If left untreated, Lyme disease can cause severe swelling and inflammation of the joint, cardiac complications, and in some very rare cases CNS symptoms (more on this in a second).

It is diagnosed by an ELISA test followed by a Western blot. The reason for the additional test is that the ELISA has a high false positive rate. Particularly in endemic regions, the test can come back positive even in patients without the disease. Thus, a positive ELISA without symptoms should not be considered a definitive diagnosis of Lyme disease.

Lyme disease is totally treatable with a course of antibiotics -- usually for about a month or 6 weeks. In cases of advance Lyme, we sometimes use IV, rather than oral antibiotics.

I want to emphasize this point: there are cranks out there who are advocating long-term prescription of antibiotics for Lyme disease. This is not only totally unnecessary, it is actively dangerous. And long-term prescription of antibiotics isn't the worst thing they unnecessarily prescribe. How about some hyperbaric oxygen or hydrogen peroxide injections? Neither do a lick of good, and both might kill you. (More on that sordid business at Quackwatch.)

Specifically relating to the issue of psychiatric or mental symptoms: yes, it is true that that Lyme can have CNS symptoms. These tend to be numbness or pain in the extremities or mental status changes resulting from encephalitis such as memory loss, mood changes, or sleep disturbance. (See here and here.) These symptoms nearly always go away with treatment with antibiotics:

But I want to make something super clear: there is not a shred of evidence to suggest that Lyme disease causes violent behavior -- the "lyme rage" idea being pushed by patient advocate groups.

Basically, the idea of lyme rage is based on the idea that you can either have persistent infection with the causative bacteria or persistent symptoms after the bacteria has been eradicated. But there is no real evidence for this argument. First, there is no evidence to suggest that any of the causative bacteria survive an appropriately taken course of antibiotics:

It is highly unlikely that post-Lyme disease syndrome is a consequence of occult infection of the central nervous system. This conclusion is based on evidence such as the absence of inflammation in the cerebrospinal fluid, negative results of both cultures and PCR assays for B. burgdorferi in the cerebrospinal fluid, the absence of structural abnormalities of the brain parenchyma, and normal neurologic function, with no effect of antibiotic therapy (as compared with placebo) on cognitive function. (Citations removed.)

It is indeed true that sometimes courses of antibiotics fail to eradicate a bacteria. For example, the antibiotics could be taken incorrectly (or not at all). The patient could be immunocompromised. But once the disease is eradicated by drugs, it is gone, dead, done for.

Second, "chronic lyme disease," as the term is currently being used attributes all manner of symptoms to a persistent infection whether or not the disease was adequately diagnosed in the first place and whether or not those symptoms were from a pre-existing condition. This caused a review of the subject (same as above) to deride it as non-medical hooey:

This term is used by a small number of practitioners (often self-designated as "Lyme-literate physicians") to describe patients whom they believe have persistent B. burgdorferi infection, a condition they suggest requires long-term antibiotic treatment and may even be incurable. Although chronic Lyme disease clearly encompasses post-Lyme disease syndrome, it also includes a broad array of illnesses or symptom complexes for which there is no reproducible or convincing scientific evidence of any relationship to B. burgdorferi infection. Chronic Lyme disease is used in North America and increasingly in Europe as a diagnosis for patients with persistent pain, neurocognitive symptoms, fatigue, or all of these symptoms, with or without clinical or serologic evidence of previous early or late Lyme disease. (Citations removed.)

And later:

Chronic Lyme disease is the latest in a series of syndromes that have been postulated in an attempt to attribute medically unexplained symptoms to particular infections. Other examples that have now lost credibility are "chronic candida syndrome" and "chronic Epstein-Barr virus infection." The assumption that chronic, subjective symptoms are caused by persistent infection with B. burgdorferi is not supported by carefully conducted laboratory studies or by controlled treatment trials. Chronic Lyme disease, which is equated with chronic B. burgdorferi infection, is a misnomer, and the use of prolonged, dangerous, and expensive antibiotic treatments for it is not warranted. (Citations removed.)

The second, and in my opinion, much more compelling argument that this shooting was not caused by Lyme disease is one of parsimony. There is a long, long list of organic causes for violent psychosis -- some of them infectious. Before you can attribute this man's -- or anyone else's -- violence to Lyme disease -- an argument for which there is little or no evidence -- you have to rule out the alternative medical causes for which we have substantial clinical evidence. The differential diagnosis of psychosis includes:

  • Infectious causes: neurosyphilis, AIDS, herpetic encephalitis,
  • Substance abuse: PCP, alcohol, methamphetamine, hallucinogens, barbituates, ketamine
  • Metabolic causes: acute intermittent porphyria, B12 deficiency, heavy metal poisoning
  • Neurological disorders: epilepsy, brain damage due to stroke or trauma, Wilson's disease, mad cow disease, Wernicke-Korsakoff syndrome, Lupus, Huntington's, and many, many others
  • Psychiatric disorders: bipolar, schizophrenia, etc.

Schizophrenia is underlined because it is absolutely first on the differential for violent psychosis, particularly if it includes paranoid delusions.

My point is that if this guy's lawyer wants to assert that Lyme disease caused this, he is asking us to believe the long bomb of the century. There are plenty of significantly more common things that cause a psychotic break. And there is one really more common thing that causes violence: the nature of the human species.

Before he can convince me that some occult brain damage caused by Lyme disease, I want to see some evidence that it wasn't something else on that list. This guy has done a bad, bad thing, and it looks like he is going to pay for it regardless of what is wrong with him. Having never met the guy, I don't know whether or not there is something medical causing this.

But it isn't Lyme disease.


Just to round out this post and convince you that I am not alone in thinking this, here is an interview with a Lyme specialist on the case from WebMD:

"I don't know of any convincing evidence that Lyme disease can cause violence or psychosis," Gary Wormser, MD, tells WebMD. Wormser is director of the Lyme Disease Center and chief of infectious diseases at New York Medical College in Valhalla, N.Y.

"We can be clear Lyme disease does not lead to psychotic and violent behaviors," William Schaffner, MD, tells WebMD. Schaffner is president-elect of the National Foundation for Infectious Diseases and chair of preventive medicine and infectious diseases at Vanderbilt University in Nashville, Tenn.

In an August 2008 article -- written before the alleged attack by Terry J. Sedlacek -- the St. Louis Post-Dispatch chronicled the man's decade-long mental health problems. The article suggested his symptoms were due to Lyme disease.

But such "chronic" Lyme disease is "not a sound diagnosis" for anyone, Schaffner says. Untreated Lyme disease certainly can go on for a very long time. And Lyme disease damage doesn't necessarily go away with treatment. But Schaffner says there is little evidence that prolonged antibiotic therapy -- or other radical, unproven treatments -- benefits patients.

"The history I've gleaned from the news reports suggests this man was being treated for supposed chronic Lyme disease, a diagnosis that needs to be looked at with great skepticism," Schaffner says. "If this was a misfocused attention on Lyme disease, his real underlying problem was not given attention and therapy. Because Lyme disease, in whatever manifestation, does not lead to violent and psychotic behavior."

Wormser has actually looked for Lyme disease in Missouri, near the Illinois border where the man was supposed to have contracted the disease.

"In that part of Illinois, that this person lived in, it would be almost unheard of to have true Lyme disease," he says. "But so many people get misdiagnosed because of doctors sending samples to labs that give unreliable results. I would not be surprised if this individual were misdiagnosed."

But even if the man did have Lyme disease, the evidence suggests it could not have been responsible for his recent behavior.

UPDATE: I am going to make this clear because I know it is going to be a problem with this post. I will only tolerate genuine attempts to understand the science of this disease in the comments. If it degenerates into ad hominem attacks or attempts to justify pseudoscience, I will delete your comment.

Go sell crazy somewhere else. We are all stocked up here.

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thank you - those who tried to argue with these Yale folks. i know how frustrating it must be. remember, the theory that a bacteria (rather than stress or poor eating habits) could cause ulcers was ridiculed. i have lyme, rash misdiganosed as psoriasis, late treatment, and before i was finally diagnosed, i had CNS manifestations so frightening -i was certain i had ALS. i trembled and twitched and raged and was linguistically and cognitively impaired. my list of diagnoses prior to the long term abx cure were chostochondroitis (sp?), leukopenia,lumbar radiculitis, bilateral thumb arthritis, elbow tenosynovitis, elevated cardiac enzymes , snapping scapula syndrome, shoulder tendonitis, ankle arthritis, etc etc i can afford to get treatment outside of insurance approved treatment. what these yale people do is deny approriate treatment for those who need long term abx but must rely on insurance approved conventional treatment and these people just get sicker and sicker. God forgive the Yale folks.

By Denise D. Cordes (not verified) on 15 Mar 2009 #permalink

Jake,

I have an idea....Why don't you infect yourself with Lyme Disease, and wait a couple of years to get treatment, and see if it clears up with a few weeks of antibiotics.

I think if you did this you might change your views a little bit.

Hi Jake,
I just thought I'd share some information with you. This is Russel Johnson's patent for the very first lyme vaccine: US PATENT 4,721,617---"The chronic forms of the disease such as arthritis (joint involvement), acrodermatitis chronica atrophicans (skin involvement), and Bannwart's syndrome (neurological involvement) may last for months to years and are associated with the persistence of the spirochete. A case of maternal-fetal transmission of B. burgdorferi resulting in neonatal death has been reported. Domestic animals such as the dog also develope arthritis and lameness to this tick-borne infection. For every symptomatic infection, there is at least one asymptomatic infection. Lyme disease is presently the most commonly reported tick-borne disease in the United States." "The infection may be treated at any time with antibiotics such as penicillin, erythromycin, tetracycline, and ceftriaxone. Once infection has occurred, however, the drugs may not purge the host of the spirochete but may only act to control the chronic forms of the disease. Complications such as arthritis and fatigue may continue for several years after diagnosis and treatment." The IDSA has always known this! This was their argument to get funding for the vaccine,they knew it could become chronic.

CDC admits ceftriaxone fails to eradicate all spirochetes: Persistence of Borrelia burgdorfei following antibiotc treatment in mice--Emir Hodzic, Sunlian Feng, Kevin Holden, Kimberly J. Freet, and Stephen W. Barthold-Centers for Comparative Medicine, Schools of Medicine and Veterinary Medicine, University of California at Davis, One Shields Avenue, Davis, CA 95616;

The effectiveness of antibiotic treatment was examined in a mouse model of Lyme borreliosis. Mice were treated with ceftriaxone or saline for one month, commencing during the early (3 weeks) or chronic (4 months) stages of infection with Borrelia burgdorferi. Tissues from mice were tested for infection by culture, PCR, xenodiagnosis, and transplantation of allografts at 1 and 3 months after completion of treatment. In addition, tissues were examined for spirochetes by immunohistochemistry. In contrast to saline-treated mice, mice treated with antibiotic were consistently culture-negative, but tissues from some of the mice remained PCR-positive, and spirochetes could be visualized in collagen-rich tissues. Furthermore, when some of the antibiotic treated mice were fed upon by Ixodes scapularis ticks (xenodiagnosis), spirochetes were acquired by the ticks, based upon PCR, and ticks from those cohorts transmitted spirochetes to naive SCID mice, which became PCR-positive, but culture-negative. Results indicated that following antibiotic treatment, mice remained infected with non-dividing but infectious spirochetes, particularly when antibiotic treatment was commenced during the chronic stage of infection. I guess Mousehausen's is now official!

I'll be sending some more studies from the IDSA. Talk to you soon!

Janis Krause

By Janis Krause (not verified) on 17 Mar 2009 #permalink

Thank God , you , Jake Young , and the likes of you in the medical community arent the only source of medical help for people who have contracted the borrelia bacteria , had it for a long time before getting antibiotics , and not gotten well after the standard 3 week doxycycline prescription...I tremble when I think about how it would be if the only Dr. I had to turn to was somebody like you.
Would be good if you contracted Borrelia , and went with it for months before getting treatment , and still felt like shit after your standard treament.

Borrelia sufferer

Wow. You're a retard for a doctor. For someone who has is PRACTICING medicine and should understand that the idea of LEARNING about how to treat patients about diseases is always in your oath. To say that Lyme Disease isn't chronic is ridiculous. Let's just take all of the evidence that has been compiled in the last thirty to forty years about the disease and look at it.

Oh, and let's not forget about the conference where it was shown to the world that the disease has a biofilm. Know what that is, Mr. Big-shot-Doctor? Yeah, it's proof that the disease can become a chronic illness. Not surprising given the fact that Lyme Disease is similar to Syphilis. Maybe you should do some research before posting like an idiot. The people who wrote the Lyme Disease Protocol a few years back stating that it can be treated in two weeks are under investigation from the District Attorney of Connecticut. Wonder why.. oh, that's right, influence of MONEY from the patients they've benefited from as well as influence from insurance companies.

Yeah, good job on your text book answer. I hope you got an A in college. Too bad you obviously aren't smart enough to make your own deductions and look through the bullshit in life, Mr. Hot-Shot Hero.

Hey, with any luck, the guy will die and everyone can get his brain sliced up and evaluated to prove or disprove theories. I read the Associated Press article you link to and it factually reports the position of his family. Its not the "Huffington Post" position, its his family's position.

Your comment - "(And, shocker: this interpretation of the story is being pushed over at Huffington Post)" is misleading.

Kathy,

The title of the Huffington Post article is: "Ticking Time Bomb (Literally): Man who Murdered Pastor Was Profiled by Paper Last Summer as Lyme Disease Victim."

If the author did not believe that it explained the assailants behavior, why did he describe him as a "ticking time bomb." I think the title makes clear that the Huffington Post position is the family's position.

there are now a multitude of scientific peer reviewed studies proving persistence of infection and symptoms and their sequaliae.
there are now ample refutations to your conjecture

I understand your lack of medical expertise but please dont simply assume what you see from Wormser et al and the IDSA to be true--the very prestigious Columbia University Medical Center's brain fallon is a psychiatrist with reams of files from Lyme patients that indeed do manifest psychiatric symptoms that magically disappear with only longer antibiotic treatments. Those with simliar psych manifestations and No Lyme do not improve with antibiotics and require psych meds

please stop minimizing a serious situation of politics and innuendo. Many are ill and too many are undiagnosed and undertreated due to your continuance of this sort of ignorance

upon request Ill be more than happy to give you all the citations you care to read--alas I figure you dont care at all

By Finette Russak (not verified) on 10 Mar 2009 #permalink

"there are now a multitude of scientific peer reviewed studies proving persistence of infection and symptoms and their sequaliae.
there are now ample refutations to your conjecture"

Would you mind providing us with some?

I think we do care, Finette... why not include a few links or citations since there are "reams" of them?

By mezzobuff (not verified) on 11 Mar 2009 #permalink

Here are just a few studies showing that Lyme often persists despite aggressive antibiotic treatment. Would be good to do some research before making statements to the contrary. As is typical, those who are the most adamant are the most uniformed and the least interested in the facts.

Evidence of Persistent Infection

Evidence of persistent infection notwithstanding previous antibiotic treatment is strong. B. burgdorferi have been
cultured from patients who have been given intensive, 21 days to one year, antibiotic therapy with IV third
generation cephaloporins. A summary of some of the peer-reviewed medical research demonstrating
persistence of B. burgdorferi is set forth in the table below.
Laboratory Confirmed Infection with Borrelia burgdorferi (Bb) Despite Antibiotic Treatment

Study Comments

Battafarano et al.
19931
Patient with chronic septic Lyme arthritis of the knee for 7 years, despite multiple antibiotic
trials and synovectomies. Bb documented in synovium and synovial fluid.

Bayer 19962 97 patients who had been treated with antibiotics for extended periods of time and had
symptoms of chronic Lyme were PCR-positive.

Bradley et al.
19943
Two previously treated Lyme patients with PCR-positive synovial fluid.

Breier et al.
20014
Despite treatment with four courses of ceftriaxone, â[s]pirochaetes were isolated from skin
cultures obtained from enlarging LSA lesionsâ¦. [S]erology ⦠was repeatedly negative.â

Haupl et al.
19935
Repeated antibiotic treatment necessary to stop the progression of disease but did not
completely eliminate Bb from all sites of infection. Bb cultured from ligament sample.

Lawrence et al.6 Patientâs CSF was positive for complexed anti-B. burgdorferi antibodies, B. burgdorferi nucleic
acids and free antigen despite aggressive antibiotic therapy.

Liegner et al.
19937
11 months later, after treatment, T-cell stimulation test with Borrelia burgdorferi antigens were
strongly positive. A year later, paired serum and CSF samples were strongly positive.
Masters 19958 Patient treated for six months; then relapsed and Borrelia burgdorferi was cultured from blood.

Nocton et al.
19949
Of 19 Lyme arthritis patients treated with either parenteral antibiotics or long courses of oral
antibiotics, PCR confirmed Borrelia burgdorferi detected in synovial fluid of 37% of patients.

Nocton et al.
199610
Bb DNA was detected in CSF samples of 11 (25%) of 44 with chronic neuroborreliosis.
Significant correlation between PCR results and the duration of previous intravenous
antibiotic therapy.

Oksi 199911 40% (13 of 32)) patients had clinical relapses that were PCR or culture-confirmed.

Pfister et al.
199112
âIn one patient Borrelia burgdorferi was isolated from the cerebrospinal fluid 7.5 months after
ceftriaxone therapyâ¦. [P]rolongation of therapy may be necessary.â
Preac Mursic
199613
Borrelia burgdorferi was isolated by culture in 5 patients, 4 of whom had previously tested
antibody-negative.

Preac-Mursic
199314
Patient with blurred vision treated with two separate month-long cycles of tetracycline had
symptoms persist for several years. Borrelia burgdorferi cultures from iris biopsy.

Priem et al.
199815
Although âPCR⦠was negative in synovial fluid and urine,â PCR confirmed Borrelia
burgdorferi in synovial membrane of 4 previously treated patients with Lyme arthritis.

Schmidli et al.
199816
Borrelia burgdorferi was cultured from joint fluid after treatment.
Compiled by California Lyme Disease Association - www.lymedisease.org - 2008
Animal studies

Straubinger et al.
199717
30 days treatment âdiminished but failed to eliminate persistent infectionâ in dogs. Antibody titers fell,
but âafter antibiotic treatment was discontinued antibody levels began to rise again, presumably in
response to proliferation of the surviving pool of spirochetes.â

Straubinger 200118 All 8 infected dogs previously treated with 30 days antibiotics were PCR positive from tissue samples
after necrosis. 25 tissue samples per dog were used.

Hodzik et al.
200819
â[F]ollowing antibiotic treatment, mice remained infected with nondividing but infectious
spirochetes.â

REFERENCES
1 Battafarano DF, Combs JA, Enzenauer RJ, Fitzpatrick JE. Chronic septic arthritis caused by Borrelia burgdorferi. Clin Orthop, 1993; 297:238-
41.
2 Bayer ME, Zhang L, Bayer MH, Borrelia burgdorferi DNA in the urine of treated patients with chronic Lyme disease symptoms. A PCR study
of 97 cases. Infection, 1996; 24(5): p. 347-53.
3 Bradley JF, Johnson RC, Goodman JL. The persistence of spirochetal nucleic acids in active Lyme arthritis. Ann Intern Med, 1994; 120(6): p.
487-9.
4 Breier F, Khanakah G, Stanek G, Kunz G, Aberer E et al. Isolation and polymerase chain reaction typing of Borrelia afzelii from a skin lesion
in a seronegative patient with geereralized ulcertating bullous lichen sclerosus et atrophicus. 2001. Br J Dermatol, 144(2):387-392.
5 Haupl T, Hahn G, Rittig M, Krause A, Schoerner C, Schonnherr U, et al. Persitence of Borrelia burgdorferi in ligamentous tissue from a patient
with chronic Lyme Borreliosis. Arthritis Rheum, 1993; 36:1621-1626.
6 Lawrence C, Lipton RB, Lowy FD, Coyle PK. Seronegative chronic relapsing neuroborreliosis. Eur Neurol 1995;35(2):113-7.
7 Liegner K, Rosenkilde C, Campbell G, Quan T, Dennis D. Culture confirmed treatment failure of cefotaxime and minocycline in a case of
Lyme meningoencephalomyelitis. Abstract #36, Fifth International Conference on Lyme BorreliosisâArlington, VA 1992.
8 Masters E. Spirochetemia after continuous high-dose oral amoxicillin therapy. Infec Dis Clin Pract, 1995; 3(3):.207-208.
9 Nocton, JJ, et al. Detection of Borrelia burgdorferi DNA by polymerase chain reaction in synovial fluid from patients with Lyme arthritis. N
Engl J Med, 1994; 330(4): p. 229-34.
10 Preac-Mursic V, et al. Formation and cultivation of Borrelia burgdorferi spheroplast L-form variants. Infection, 1996; 24: p. 218-26
11 Oksi J, et al., Borrelia burgdorferi detected by culture and PCR in clinical relapse of disseminated Lyme borreliosis. Ann Med, 1999. 31(3): p.
225-32.
12 Pfister HW, Preac-Mursic V, Wilske B, Schielke E, Sorgel F, Einhaupl KMJ. Randomized comparison of ceftriaxone and cefotaxime in
Lyme neuroborreliosis. J Infect Dis 1991;163:311â8.
13 Preac-Mursic V, et al. Formation and cultivation of Borrelia burgdorferi spheroplast L-form variants. Infection, 1996; 24: p. 218-26.
14 Preac-Mursic V, Pfister HW, Spiegel H, Burk R, Wilske B, Reinhardt S, Bohmer R. First isolation of Borrelia burgdorferi from an iris biopsy. J
Clin Neuroophthalmol 1993;13:155â61.
15 Priem S, Burmester GR, Kamradt T, Wolbart K, Rittig MG, Krause A. Detection of Borrelia burgdorferi by polymerase chain reaction in
synovial membrane, but not in synovial fluid from patients with persisting Lyme arthritis after antibiotic therapy. Ann Rheum Dis
1998;57:118â21.
16 Schmidli J, Hunzicker T, Moesli P, Schasd UB. Cultivation of Borrelia burgdorferi from joint fluid three months after treatment of facial palsy
due to Lyme borreliosis J. Infect Dis 158 (1988) 905-906.
17 Straubinger RK, Summers BA, Chang YF, Appel MJ. Persistence of Borrelia burgdorferi in experimentally infected dogs after antibiotic
treatment. J. Clin. Microbiol 1997; 35:111-116.
18 Straubinger RK. PCR-Based quantification of Borrelia burgdorferi organisms in canine tissues over a 500-Day postinfection period. J Clin
Microbiol, 2000; 38(6): p. 2191-9.
19 Hodzic E , et al. Persistence of Borrelia burgdorferi following

By Kent Holtorf, MD (not verified) on 11 Mar 2009 #permalink

Just glancing through (I have neither the time nor the desire to go through with a fine tooth comb), you cite a lot of tests that are using either PCR or serology (read: ELISA) to establish a diagnosis of persistent infection. That is not the way these tests work. Both PCR and ELISA are prone to false positives. PCR can be contaminated, and all resulting products should be sequenced to confirm diagnosis (simple amplification is not sufficient). ELISA can get false positives from a variety of related diseases as well as autoimmune.

Definitive diagnosis of Lyme disease requires both ELISA and Western positive AND the presence of Lyme symptoms. For more on this testing paradigm, read this FDA advisory:

http://www.fda.gov/cdrh/lyme.html

Second, you do know how immunity works, right? Individuals previously exposed to the bacteria are likely to be seropositive even if they never showed symptoms of the disease. This means that a large percentage of individuals who lived in the Northeast may test positive.

Third, you cite some case reports with individuals with pre-existing conditions. How do you prove that it wasn't that, that caused their symptoms?

Four, in science we use statistics. You are going to have to do better than case reports because controlled studies of large numbers of people done on the subject have A) failed to find persistent infection and B) failed to show differences as the result of long-term antibiotic usage in sufferers of "chronic lyme."

Five, I care. I care about patients getting accurate diagnoses and not being pushed into unnecessary and dangerous treatments by cranks. I write this stuff because I care.

Also, there doesn't seem to be anything in that list suggesting a link between Lyme disease and violence, even if the infection were persistent.

I'm not sure why I am wasting my time posting here, since you have already made up your mind. And, it appears you have bought the line propagated by IDSA hook, line and sinker. Do you ever stop to acknowledge or ponder the corruption in academic medicine?

As a Yale-trained psychiatrist who practiced psychiatry on Cape Cod, I am very aware that Lyme disease can cause a multitude of neuropsychiatric symptoms, many reports which have not been published because most of the editorical board of the major medical journals are controlled by those who automatically embrace the "business mode" of Lyme disease propagated by organizations such as IDSA. The vast majority of physicians have little knowledge of what the real disease looks like because the doctors with vaccine agendas, and ties to pharmaceutical houses got their first.

A had a very large psychiatric practice on Cape Cod that was full of Lyme disease patients. There is no question in my mind that this case could have been caused by untreated Lyme disease. Did I learn this in my residency? No. I believe that the tight cadre of physicians who control publications in the US on Lyme disease do not want physicians or the American public to understand the breadth and depth of this epidemic, and the forms of pathology that it may take.

To do so would interfere with their business agendas related to this disease. Both Dr. Steere and Dr. Wormser have admitted to doing consulting work on LD vaccines. In order to commercialize a LD vaccine there are many aspects of the real disease that don't fit the business model. So, instead of truly investigating the disease -- doing the research that needs to be done to truly understand the pathogenesis of the disorder -- they simply say, "it's something else."

Do they care about anything else other than their commercial projects staying on track? One has to wonder.

Lynn Shepler MD JD

By Lynn Shepler MD JD (not verified) on 11 Mar 2009 #permalink

Quoting a CNN article, In a 2002 study in Czech Republic 36% of 900 psychiatric patients had antibodies to the bacterium linked to lyme disease versus 18% of the 900 healthy control subjects. They recruited more than 900 psychiatric patients admitted to the Prague Psychiatric Center between 1995 and 1999 for their study. About a third of the patients had anxiety disorders, a third mood disorders, a quarter schizophrenia or other psychotic diseases, and the remaining subjects personality disorders, delirium, dementia, or other conditions. All of the patients agreed to have samples of their blood screened for antibodies to Lyme disease. The researchers also selected some 900 healthy subjects to serve as controls. 36% and 18% is a highly significant difference and it links lyme disease to psychiatric disorders. There is also a highly respectable study going on at columbia university that I went to to get neurological tests and brain scans by Dr. Brian Fallon. It showed that the lyme disease did indeed go to my brain and showed signs of encephalitis.. dont shoot ur mouth off if u dont know the facts. This is a terrible disease that has so many symptoms. Right now there is a huge debate going on between two Lyme groups and the patients are the ones suffering right now. Do not assume that your right, I am not defending the shooter but do not assume that once u heard one side of the argument you heard everything.