In a new video published on the Centers for Disease Control and Prevention (CDC) YouTube page about two weeks ago, the federal health agency advises that if being diagnosed with Lyme disease and having received treatment you don’t feel better, get a second opinion because you may not have the tick borne disease.
The video tells the story of Robert, who after being diagnosed with chronic Lyme disease after demonstrating a history of joint pain/stiffness, memory loss, and numbness and tingling in both hands and being treated with long term antibiotics, got worse and not better.
In time, he eventually began to lose sight in his right eye.
Subsequent doctor visits with a neurologist revealed that instead of chronic Lyme disease, Robert had a pituitary tumor.
He now suffers with permanent damage musculoskeletal changes, heart and kidney issues.
The CDC’s message in the video is: If you’ve had treatments for Lyme disease and still don’t feel better, please get a second opinion. An incorrect diagnosis can lead to permanent damage or death.
It is not clear from the video how rare or common situations like this occur.
1989 IDSA journal reviews of infectious disease vol I I supplement 6 sept- October calls Lyme disease the great imitator and can also be confused with appearance of cancerous tumors! Read this journal it will make your hair stand up!
Many people with CONFIRMED Lyme disease do not get well with treatment. If you have Lyme disease for a long time before diagnosis, it is very difficult to treat and many people end up with life long chronic illness. People are misdiagnosed all the time, this is not unique with Lyme disease. It is possible to be misdiagnosed, but it is just as possible to have chronic Lyme disease.
Interesting that he mentions doctors saying, “It’s all in your head,” because a physician well-versed in tick-borne disease would have never said that. And the tick-borne disease docs I have spoken to would have always kept other possibilities in the differential diagnosis. And they certainly would have referred a patient with sudden-onset optical symptoms to an ophthalmologist! So while this video may be attempting to cast aspersions on “Lyme literate” physicians, it mostly just reinforced what such physicians already know. And I would agree — ALWAYS keep other diagnoses in mind, especially if t the treatment isn’t working.
We have been dealing with an antibiotic resistant superbug purposely concealed to promote vaccine development and it has become blatantly obvious that the CDC will go to great lengths to insure that Lyme disease remains within its narrow definition in order to fit the vaccine model. A chronic relapsing disease does not fit the vaccine model and post-treatment Lyme disease syndrome is simply a fabricated medical condition disguising treatment failure.
The Principle Investigators of the two previous Lyme vaccines: Allen C. Steere for SmithKlineBeecham’s LymeRix and Gary Wormser for Connaught’s vaccine (which never made it to market) have conceptualized a disease that would enable vaccine development. The one-size-fits-all Lyme treatment guideline (lead author: Gary Wormser) matches the conceptualized disease. A preventive vaccine for Lyme disease would not satisfy the FDA if a chronic persistent infection and seronegative disease exist.
If you are finding this difficult to digest I suggest you review the petition calling for a congressional investigation into the deliberate mishandling of Lyme disease as there are 25,500 signatures and 350 pages of heart wrenching comments from disabled Lyme patients across the globe.
https://www.change.org/p/the-us-senate-calling-for-a-congressional-investigation-of-the-cdc-idsa-and-aldf/u/4568480
Persistent Lyme infection: 273 Peer-Reviewed Studies
http://home.comcast.net/~runagain/Persistence%20of%20Lyme%20Disease.doc
Congenital Transmission of Lyme: 28 Peer-Reviewed Studies
http://home.comcast.net/~runagain/Congenital%20Transmission%20of%20Lyme.doc
Seronegativity in Lyme borreliosis: 103 Peer-Reviewed Studies
http://www.lymeinfo.net/medical/LDSeronegativity.pdf
Carl Tuttle
Hudson, NH
Carl thank-you for your petition. You have so concisely defined the battle ground for this disease. It is big Pharma, determined to mine the billion dollar vaccine market.
And the absolute reverse is even truer. If you see ai fectious disease doctors, neurologists or any soecialist who follows the ignorant CDC/IDSA, get as many opinions as you can u til yiu are safely in the hands of an LLMD. My daughter was misdiagnosed for 13 of her 15 yrs with Lyme, amd was told she needed hip surgery, that she was faking neuropsyche tests, that it was depression…all the while it was encephalopathy from tertiary stage untreated Lyme and it was the LYME dr who order her brain spect and a noted neurologist ordered a Pet scan and Pet MRI. She couldn’t get out of bed for a year, and finally once in IV Her Hashimotos disappeared, she has so far reversed the frontal, and occipital lve damage, the hypometabolism in her cerebellum has decreased while it is gone from the frontal, parietal and coccipital lobes. The hypoperfusion is reversed in the frontal,lobe and she still has a ways to go on her temporal lobe and basal ganglia. The lint is 28 days would not have done a thing. She is on IV 9 months and in college, up for 8 am classes three times a week, going to recitations at nights writing papers and part of clubs. She would have been dead at the hands of mainstream morons who hate Lyme drs. I hope and pray the CDC, the IDSA and their family members get this insidous disease and they suffer the way all Lyme patients are! They need to be sued for all this BS they out out there and the lives they are ruining. And as for going blind? My daughter lost sight in one eye temporarily because of the horrific head and eye pressure from the Lyme encephalopathy,,and once she got on IV, it all lifted. This confirmed with imaging studies and blood work, so nothing is in my daughter’s head, except the literal disease!
Maple370,
I would love to know who is treating your daughter. My dr. feels certain that I have Lyme even though I have had 3 Lyme tests where 2 were neg. and 1 was “inconclusive”. She is not a Lyme specialist and only knows to treat with oral Abx. I think I have had it a very, very long time, probably since childhood. I need someone who knows this disease and how to treat it. I am so glad that your daughter is doing well. I hope that she continues to improve and tell her story so that others may seek help for Lyme. Thank you so much!
Lyme disease can cause pituitary tumors. They are inflammatory and called secondary hypophysitis and they resolve with IV antibiotics. Treatment for secondary hypophysitis is aimed at treating the underlying condition.
http://www.ncbi.nlm.nih.gov/pubmed/19945028
Best Pract Res Clin Endocrinol Metab. 2009 Oct;23(5):639-50. doi: 10.1016/j.beem.2009.05.009.
Pituitary tumours: inflammatory and granulomatous expansive lesions of the pituitary.
Inflammatory lesions are unpredictable and can expand and shrink. They do not tell us what kind of tumor in this video. An infectious or inflammatory lesion is actively destroying the pituitary as long as the underlying illness goes untreated; they can appear and disappear and get big really fast. The solution is curing the systemic infection with IV antibiotics.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3183529/
Hypothalamic pituitary dysfunction in acute nonmycobacterial infections of central nervous system
Infectious diseases of the CNS may cause hypothalamic and/or pituitary dysfunction. Reports of anterior pituitary dysfunction following infectious diseases of the CNS are rare, and the incidence has not yet been studied systematically. Most of these studies have been reported following viral meningoencephalitis. The earliest such case reports came from Hagg et al, who reported two cases of persistent hypothalamic pituitary insufficiency (HPI) following acute viral meningoencephalitis due to Coxsachie B5 virus.[3] Subsequently Kupari et al, reported HPI following Influenza A and Herpes Simplex meningoencephalitis.[4] In a larger case series, HPI was studied in 19 patients following 10–56 after acute CNS infection.[5]
Of all these patients, four suffered from neuroborreliosis, two from encephalitis (two tick-borne encephalitis), and 13 from meningitis (one herpes simplex, one varicella, one enterovirus, 10 of unknown origin)
The authors concluded that isolated or combined pituitary deficiencies, which could present at the acute phase and/or occur at a later stage, can develop in a considerable proportion of patients after acute infectious meningitis.
The results showed that 32 (42.7%) cases showed relative or absolute cortisol insufficiency. Twenty-three (30.7%) cases showed central hypothyroidism and 37 (49.3%) cases had hyperprolactinemia.
The possible mechanisms of HPI in TBM are direct involvement of pituitary gland, vasculitis, or/and basal meningitis.
In conclusion, hypothalamic pituitary hormonal dysfunction is not uncommon in newly diagnosed patients with acute nonmycobacterial meningitis. The most common hormonal abnormalities seen were adrenal insufficiency and hyperprolactinemia. Further studies are needed to evaluate PHA using dynamic pituitary tests and MRI in subjects with acute CNS infections.
p Laboratory assays for the diagnosis of neuroborreliosis are of limited clinical value [151, 222 ]. page 75 http://www.idsociety.org/uploadedFiles/IDSA/Guidelines-Patient_Care/PDF_Library/Laboratory%20Diagnosis%20of%20Infectious%20Diseases%20Guideline.pdf