Hormone restoration

HOW DR. LINDNER'S DAUGHTER'S DISABLING ILLNESS FORCED HIM TO LEARN THAT CHRONIC BABESIOSIS EXISTS AND IS CAUSED BY THE SEQUESTERING SPECIES BABESIA ODOCOILEI

For more explanation of this disease and its treatment, see Dr. Lindner's 2021 powerpoint presentation (recently edited). It was given at the annual conference of the International Lyme and Associated Diseases Society (ILADS).

See UPDATE on his daughter's death from hemophagocytic syndrome below.

When his eldest daughter, Valerie, was 10 years old, Dr. Lindner removed two partially engorged Ixodes scapularis (deer) ticks from her ear and neck. She had no subsequent fever or rash, so he gave her no prophylaxis--as per the CDC and Infectious Diseases Society of America guidelines. She later reported that within a few months she became depressed and found it difficult to draw or communicate with friends online. By age 14 she was depressed and suicidal. She seemed improved while taking college courses for several years, but her cognitive dysfunction and intolerance of mental exertion gradually worsened with time. With the stress of full-time classwork at a university, she worsened, but improved somewhat with the help of natural desiccated thyroid (NDT). However, she continued to worsen with time. Lyme tests were negative. Corticosteroid courses left her in a worse state. By the age of 24, she was mentally, emotionally and physically disabled.

At that time, in mid-2018, testing at IGeneX for Lyme disease, Babesia spp., Bartonella spp., and Ehrlichia was negative. Magnetic resonance imaging (MRI) of her brain revealed scattered white matter hyperintensities, rarely seen in young adults. A neurologist suspected multiple sclerosis, but Dr. Lindner and Valerie thought a chronic infection to be much more likely and consulted a local Lyme-literate medical doctor (LLMD). Empiric antimicrobial therapy with doxycycline, then other antibiotics and antimalarials produced flu-like symptoms and mental distress and left her in a worse state. She especially could not tolerate any antimalarial medications (atovaquone, hydroxychloroquine, artemisinin/artesunate) as they greatly worsened her mental pain--which she described as an unbearable feeling of all negative emotions rolled up into one. Venous blood smears were negative for Babesia. She tested positive for an ongoing Bartonella henselae infection by FISH and antibodies, but 9 months of treatment for this caused continuous herxing without improvement. “Herxing” refers to the Jarisch-Herxheimer reaction seen with the treatment of syphilis. It is a succinct and useful colloquialism for “Herxheimer-like reaction”—the increased immune reaction that occurs when any immune-evading parasites are killed by anti-microbials and exposed to the immune system.

Repeat testing at IGeneX was positive for Babesia sp. infection by FISH--showing that she had an active Babesia species infection. She also had IgM antibodies to Babesia duncani. She had no B. microti antibodies--the species that infectious disease authorities believe to be the cause of almost all human babesiosis. B. microti produces only an acute illness--not a chronic infestation. (IGeneX has found ongoing Babesia infestation in thousands of persons with their FISH test, but mainstream infectious disease authorities have ignored this fact.) A positron emission tomography (PET/MRI) scan of her brain revealed marked regional metabolic abnormalities consistent with an inflammatory or autoimmune encephalitis. She again tried to take antimalarials to treat her babesiosis, but could not tolerate them. Desperate for help, they tried to reduce her reactivity to the Babesia with low-dose immunotherapy. It produced clear improvements at times, but she flared with increasing antigen strengths and was left worse off. They consulted another neurologist who diagnosed seronegative autoimmune encephalitis, but 5 days of high-dose intravenous methylprednisolone only worsened her condition. She became much more ill during withdrawal from the corticosteroid. She could not take walks outside or watch videos with her family as such activities caused severe mental pain. She had to start taking higher and higher corticosteroid doses to survive each day--to be able to sleep, get out of bed, and eat. By this time Dr. Lindner had consulted with many LLMDs, conventional Infectious Disease physicians, neurologists and psychiatrists. No one could help his daughter--their interventions had only made her worse.

In October of 2020, while she was severely ill and immunosuppressed with both corticosteroids and plasmapheresis, and knowing that Babesia species are highly resistant to antimalarials (Abraham et al., 2018), Dr. Lindner initiated aggressive antibabesial therapy with atovaquone, azithromycin, artesunate, and tafenoquine (AAAT). Valerie had marked hemolysis (destruction of red blood cells) and hemolytic anemia, accompanied by striking improvements in her mental and physical stamina, and decline in her prednisone requirement. She could again take walks outside and watch videos with her family. However, she also suffered severe derealization and depersonalization from the large Babesia die-off. She did not feel like her past or present were real. She had distorted perceptions of people and places. Her brain had clearly gone through a dramatic change.

During the subsequent 5 months on AAAT, she had continual herxing and intermittent hemolysis, with only incremental improvements. They were able to keep her prednisone requirement low with continuous antimicrobial treatment, but she was not improving significantly. She often had drenching night sweats and transient neurological symptoms. Her spleen was palpable with inspiration. Daily urine testing revealed hemoglobinuria varying from none to 3+, and proteinuria varying from negative to 2+ (100 mg/dl). There were also marked changes in urine cloudiness and color. At times it turned amber-red, dark brown-red, and even green-black (pigmenturia). Her serum liver and pancreatic enzyme levels were elevated during Babesia die-offs. After 6 months of the most aggressive antibabesial treatment ever given to a human being she was improved, but still could not do any mentally challenging activities, including any schoolwork, drawing, or driving.

In March of 2021 Dr. Lindner called the Pennsylvania Tick Lab about his daughter's positive Babesia tests. The expert there--Dr. Nicole Chinnici--stated that they had found no B. duncani in over 5000 ticks that they had tested in the last 5 years. Therefore the positive B. duncani antibody test at IGeneX was most likely an immunoassay cross-reaction with antibodies to another Babesia species. He asked her what they have found in the ticks, and she stated that they found Babesia odocoilei in 20% of the deer ticks they had tested. It is named after its host, Odocoileus virginianus, the ubiquitous white-tailed deer. Dr. Lindner, like all other doctors, had never been told that this organism was in our ticks. He had not found this fact in any information from the US Centers for Disease Control (CDC), the Infectious Diseases Society of America (IDSA), or ILADS. He reviewed the literature on this organism and found that it was one of the most highly sophisticated Babesia species, capable of producing life-long infestation in mammalian hosts. Its most closely related species, B. venatorum, is known to infect humans in Europe and China.

By studying the veterinary literature on babesiosis, Dr. Lindner learned that some Babesia species produce chronic infestation in hosts by sequestering in capillaries throughout the host. They cause the red blood cells (RBCs) that they infect to become sticky and adhere to the linings of small blood vessels and to other RBCs. They create nests that occlude the small blood vessels. They reproduce and live out their lives there--avoiding the general blood circulation and the spleen. These nests cause dysfunction and inflammation in all tissues, including the brain. The results are fatigue and multi-organ dysfunction. This kind of chronic babesiosis has been clinically described only in dogs infected with B. canis (Malherbe 1956, Sanders 1937). Dr. Lindner realized that B. odocoilei must sequester in the capillaries and venules--this was necessary to explain his daughter's chronic illness and dramatic response to aggressive antibabesial treatment.

On learning of Babesia canis’s use of fibrin bonding for sequestration (Schetters 2019) he added oral lumbrokinase (Boluoke®), a fibrinolytic enzyme, in order to break up the intravascular nests. One week later her urine again turned red-amber, and 3 weeks later green-black with higher hemoglobin and protein levels. She became more ill and required higher prednisone doses. They had to stop the treatment to reduce the hemolysis and try to lower her corticosteroid need. Repeated cycles of lumbrokinase and AAAT had the same effect, but to a lesser degree. After each cycle of nest clearing with lumbrokinase her mental and physical stamina improved. While taking lumbrokinase, her D-dimer level was elevated at 1.55 (0-0.49 mg/L FEU), indicating fibrinolysis. Clearly, exposing and killing the sequestered Babesia parasites can create a severe illness with hemolysis that is very similar to the acute babesiosis caused by non-sequestering species such as Babesia microti.

In May of 2021, she tested positive with TLab’s recently developed B. odocoilei FISH test, indicating active infection. In March of 2022, After 21 months of antibabesial therapy, a repeat PET/MRI scan revealed greatly improved metabolism in her inferior frontal, temporal and parietal lobes. She could take lumbrokinase and AART continuously (rifabutin was substituted for azithromycin for greater effectiveness and safety). On returning to graduate school part-time, the increase mental activity and strong emotions brought more blood flow to previously under-used, heavily-infested parts of her brain, killing more Babesia and clearing more nests. She again required higher prednisone doses to tolerate the resulting inflammation in her brain. Eventually, lumbrokinase no longer seemed effective and they added nattokinase to it. This brought about severe herxing with the need for higher corticosteroid doses. With repeated nest clearing cycles using lumbrokinase and nattokinase, the amount of heme and protein seen in her urine remained lower, when it did appear. Her blood counts and chemistries were usually normal when not going through a large Babesia die-off. Shockingly, after 36 months of this aggressive antibabesial regimen, her brain and other tissues were still infested with Babesia nests. Even though much improved she was still sick and partially disabled. Clearly, this fibrin-sequestering parasitic infestation is very hard to eradicate. Most persons, fortunately, are nowhere near as heavily infested as Dr. Lindner's daughter and get marked improvements early in treatment. Some get nearly complete relief of symptoms in 6 to 15 months.

From the start, Dr. Lindner has tried to inform the medical profession about this common tick-borne infection. He informed ILADS physicians through his lectures at conferences. He contacted the Pennsylvania Dept of Health, CDC, IDSA, and many academics. He submitted case reports with discussion of B. odocoilei to several journals. He spoke to a committee of the Pennsylvania Senate--which resulted in an attack by Infectious Disease doctors on his work and on ILADS. Infectious Disease experts are in denial--embarrassed and afraid. They should have anticipated this disease because B. odocoilei is found in 10 to 20% of the deer ticks throughout the eastern US and Canada. There was every reason to believe that it could infest humans and could be a sequestering species that could produce a stealth infestation that is completely unlike acute babesiosis caused by B. microti. For years, IGeneX laboratory in California has had a FISH test that can detect Babesia species' RNA in the blood, and a B. duncani antibody test that cross-reacts with B. odocoilei antibodies. In 10,000 patient samples sent to them, they found evidence of Babesia infection in 37.5%, vs. just 31% for Lyme disease. These results were not caused by Babesia microti, which does not sequester, causes a short-lived infection, and is present in only 2% of deer ticks. Because it does not sequester, B. microti can be seen in the blood with a microscope, whereas B. odocoilei cannot be seen in blood smears. Besides IGeneX and TLab, no laboratories have any test that can detect B. odocoilei infection.

Soon after Dr. Lindner realized that the organism infecting his daughter had to be B. odocoilei, a tick expert published molecular proof of B. odocoilei infection in two persons with chronic babesiosis symptoms (Scott et al. 2021). Dr. Lindner has since found that this infection is common in his patients with fatigue, brain fog, and many other symptoms. It causes symptoms and disability that range from minimal to severe. It is the cause of much, if not most chronic fatigue and "chronic Lyme disease" and many other unexplained illnesses. Dr. Lindner and other ILADS-associated physicians are working to find additional proof of this infection and its fibrin-sequestering strategy. A top laboratory is developing a much better PCR test for B. odocoilei. This infestation will soon be common knowledge in the mainstream medical community.

UPDATE: Death from Hemophagocytic Syndrome:

His daughter's babesiosis-related symptoms and disability were gradually improving with time. During Babesia die-offs, her blood tests frequently revealed elevated markers of inflammation--high ferritin, LDH, CRP, liver and pancreatic enzymes. She required corticosteroid immune suppression continuously, and frequently needed very high doses to tolerate her inflammatory response to lumbrokinase and then lumbrokinase+nattokinase-induced Babesia nest-clearing die-offs. In November of 2023, as a result of taking high lumbrokinase and nattokinase doses for 3 weeks and dissolving more Babesia nests, she had severe inflammation and needed higher corticosteroid doses. As usual when this occurred, she stopped the lumbrokinase and nattokinase and increased her tafenoquine and artesunate doses to kill off the newly-exposed Babesia parasites and lower her corticosteroid need. At this inopportune time, she acquired a rhinovirus infection (proven by PCR testing). Within 2 days her corticosteroid need rose to unprecedented levels--twice as high as the highest daily dose that she had ever needed. She developed severe fatigue, widespread pain, and worse abdominal pain and nausea. As usual, to try to lower the high corticosteroid need, she took more strong tafenoquine doses. This worked, but when her corticosteroid need dropped precipitously, she began to have difficulty breathing and became confused.

Dr. Lindner took her to a local teaching hospital where she was found to have acute respiratory distress syndrome. Her laboratory blood tests were grossly abnormal--there were signs of liver, pancreatic, kidney and muscle damage. Her calcium, electrolyte and phosphate levels were abnormal. In the ICU she was intubated and sedated. She was essentially unconscious from then on. Her lungs were severely inflamed. She needed high oxygen levels and pressures to maintain her blood oxygen levels. Her skin began breaking down in many places. Dr. Lindner informed her physicians that her clinical picture and laboratory test results (including a ferritin level >25,000ng/ml) could only be explained by hemophagocytic syndrome. She met the criteria for hemophagocytic syndrome by any scale. It is the most severe, overwhelming, uncontrolled immune system reaction that exists. The immune system's cells attack not only the pathogen, but also the person's own tissues and organs. Dr. Lindner told her doctors that given her frequent need for very high corticosteroid doses in the past, she required much, much higher corticosteroid doses to control the overwhelming inflammation. However, as typically occurs in cases of hemophagocytic syndrome, her physicians delayed in making the diagnosis, wanting to see more proof. They did, however, give her the typical daily dexamethasone dose advised by some experts for hemophagocytic syndrome, but it was a small fraction of the doses that she had needed previously according to her symptoms. When her bone marrow began failing to produce red cells, white cells and platelets, the hematologist admitted that she had hemophagocytic syndrome. After 4 days in the hospital, in the last day of her life, her lactic acid level began to rise. The ICU provider was suspicious of a bowel infarction--which could have been caused by the hemophagocytic syndrome or by the multiple vasoconstricting medications she required to maintain her blood pressure. She was far too ill to undergo surgery. She expired during the morning of Dec. 9, 2023 from severe lactic acidosis. Her blood pressure dropped and her heart stopped beating. Her hemophagocytic syndrome was so severe that it is unlikely that any treatment could have prevented her death. She had also become weary of fighting this disease. An autopsy was performed. Dr. Lindner obtained tissue and blood specimens to send to a specialized laboratory for testing--hoping that in her death she can shed more light on this terrible parasitic infestation. What Dr. Lindner learned from her illness has already helped thousands of victims of this disease. Fortunately, the vast majority are much less ill than Valerie and much easier to treat.

See her obituary at: https://www.tunkhannockfuneralhome.com/obituaries/valerie-lindner