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). Also see his October 2022 ILADS presentation on his daughter's and another young woman's encephalitis caused by combined Bartonella and Babesia infections.

For much more information about Valerie's life, see http://henrylindner.net/Valerie/Valerie.html

NOTE: Valerie died in December, 2023 from hemophagocytic syndrome caused by a rhinovirus. Hemophagocytic syndrome can be triggered by infections, including babesiosis in otherwise healthy persons. Persons who are treating their chronic babesiosis are at no increased risk for hemophagocytic syndrome. Dr. Lindner has seen it occur only in a few very ill Babesia patients, after taking very strong antibabesial doses. Like his daughter, they all had such severe inflammation that they had required high-dose corticosteroid treatment before or during antibabesial treatment.

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. She developed a bizarre hunger--she was forced to eat to avoid mental and physical malaise. By age 14 she was depressed and suicidal. She had been unschooled until then. Thinking she might just need a life change, she started taking college courses part time. Her mood improved, but when she attended a university the stress of full-time classwork caused her fatigue, hunger, cold intolerance and brain fog to worsen. Her symptoms resembled hypothyroidism, and natural desiccated thyroid (NDT) treatment helped her energy and brain function. Lyme tests were negative. After a very strong emotional experience at the start of her senior year, she could not do classwork. Thinking this could be hypocortisolism, they tried physiological doses of hydrocortisone, but they paradoxically made her worse. During her finals week she found that very high hydrocortisone doses allowed her brain to function. After stopping corticosteroids when she graduated, she had extreme fatigue--was bedbound for many months. They tried many interventions without success. Eventually high doses of T3, the active thyroid hormone, gave her some energy so that she started graduate school after a year's absence. However, with the stress of classes she deteriorated. For the first time, she began to show signs of inflammation--acne-like skin lesions, higher body temperatures, and intolerance of any thyroid or DHEA supplementation. By the age of 24, she was mentally, emotionally and physically disabled. They decided so consult other physicians until they found some answers.

In mid-2018, she saw a neurologist. Her Mayo Clinic autoimmune encephalitis antibody panel was negative, but magnetic resonance imaging (MRI) of her brain revealed scattered white matter hyperintensities, rarely seen in young adults. The neurologist suspected multiple sclerosis, but Dr. Lindner and Valerie thought that a chronic infection from the tick bites was much more likely. They consulted a local Lyme-literate medical doctor (LLMD). Her tests at IGeneX for Lyme disease, Babesia spp., Bartonella spp., and Ehrlichia was negative. Empiric antimicrobial therapy with doxycycline for Lyme disease produced flu-like symptoms and mental distress and left her in a worse state. She especially worsened with taking antimalarial medications (atovaquone, hydroxychloroquine, artemisinin/artesunate). They greatly worsened physical suffering and her mental pain--which she described as an unbearable feeling of all negative emotions rolled up into one. She then tested positive for an ongoing Bartonella henselae infection by FISH at TLab and antibodies at Galaxy Diagnostics, but 9 months of treatment for this infection caused continuous herxing, severe at times, without any improvements. “Herxing” refers to the Jarisch-Herxheimer reaction seen with the treatment of syphilis. It is a succinct and useful colloquialism to describe the increased immune system reaction that occurs when any immune-evading parasites are killed by antimicrobials and exposed to the immune system.

They got a breakthrough when repeat testing at IGeneX was positive for Babesia sp. by FISH--showing that she had an active Babesia species infection--which is a tick-borne disease. She had IgM antibodies to Babesia duncani, but 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 and now TLab have found ongoing Babesia infestation in thousands of persons with their FISH test, but mainstream infectious disease authorities are still ignoring this fact.) She again tried to take antimalarials to kill Babesia parasites, but again could not tolerate them. Another neurologist ordered a positron emission tomography (PET/MRI) scan of her brain which revealed severe regional metabolic abnormalities consistent with an inflammatory or autoimmune encephalitis. Desperate for help, they worked with a doctor for 9 months to try to reduce her reactivity to the Babesia and Bartonella parasites with low-dose immunotherapy. It produced clear improvements on two occasions, but her symptoms flared with increasing antigen strengths and she was left in a worse state. Another neurologist diagnosed seronegative autoimmune encephalitis and prescribed 5 days of high-dose intravenous methylprednisolone. It did not help and 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 they had consulted with many LLMDs, neurologists and psychiatrists. An Infectious Disease consultant at a major teaching hospital opined that chronic babesiosis and bartonellosis do not exist. No one could help her, in fact every doctor's interventions had made her worse.

In October of 2020, she was severely ill. She could not walk outside or watch videos with her family. All sensory input was painful. After the high-dose corticosteroids did not work, the neurologist ordered plasmapheresis to remove antibodies from her blood. Two venous blood smears were negative for Babesia. Dr. Lindner, knowing that Babesia species are highly resistant to antimalarials (Abraham et al., 2018), took over her treatment in an effort to kill the Babesia parasites. Hoping that the immunosuppression would allow her to tolerate the killing of her parasites, he initiated aggressive antibabesial therapy with atovaquone, azithromycin, artesunate, and two 600mg doses of tafenoquine (AAAT). Valerie temporarily needed even higher corticosteroid doses (up to 600mgs of prednisone daily). After her tafenoquine doses she had severe hemolysis (destruction of red blood cells), 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 and resulting brain inflammation. 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. A later PET-MRI revealed a small hemorrhage in her left temporal lobe.

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 in over 5000 ticks they had found no B. duncani (the species to which she had IgM antibodies). She suggested that the positive B. duncani antibody test at IGeneX was an immunoassay cross-reaction with antibodies to another Babesia species. What species? 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 not been aware that this parasite was in the deer ticks. Neither the US Centers for Disease Control (CDC), the Infectious Diseases Society of America (IDSA), or ILADS had ever mentioned it. He reviewed the literature and found that it was one of the most sophisticated Babesia species, capable of producing life-long infestation in mammalian hosts. Its sister species, B. venatorum, which also infects deer, has been proven to infect humans in Europe and China.

By studying the veterinary literature, Dr. Lindner learned that some Babesia species produce chronic infestation in hosts by sequestering in capillaries throughout the body and brain. 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--largely avoiding the general blood circulation and the spleen. These nests cause dysfunction and inflammation in all tissues, including the brain. This kind of chronic babesiosis with multi-organ dysfunction has been clinically described only in dogs infected with B. canis (Malherbe 1956, Sanders 1937). Dr. Lindner realized that B. odocoilei must also 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) Dr. Lindner added oral lumbrokinase (Boluoke®), a fibrinolytic enzyme, in order to break up the intravascular nests. One week after starting it her urine again turned red-amber, and 3 weeks later green-black with high hemoglobin and protein levels. She became more ill and required higher prednisone doses. After 4 weeks they had to stop the lumbrokinase to reduce the hemolysis and try to lower her corticosteroid need. She needed high corticosteroid doses for a month afterwards. They then repeated cycles of lumbrokinase and along with the AAAT antibabesial cocktail. 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. They learned that 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. Her brain was working better. See a comparison of her 2020 and 2022 PET scans here.

She could now take lumbrokinase and AART continuously (rifabutin was substituted for azithromycin for greater effectiveness against Bartonella). In 2022 she was able to return to graduate school part-time, but 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. This quickly brought about severe herxing and need for higher corticosteroid doses. That had to stop the fibrinolytics within 2 days. When the inflammation calmed down, they restarted the two fibrinolytics. Which each cycle she could tolerate the combination for a longer time before having to stop them. 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 with nest-busting fibrinolytics, 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. They experience marked improvements early in treatment. Some get nearly complete relief of symptoms in 6 to 15 months. Some never need to add fibrinolytic enzymes.

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 in 2021 and 2022. He contacted the Pennsylvania Dept of Health, CDC, IDSA, and many academics. He submitted his daughter's and other patients' case reports 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 expected that B. odocoilei could infest humans and be a sequestering species that could produce a stealth infestation. They were blind to the possibility since the CDC had defined babesiosis by the acute, obvious, and short-lived infection with Babesia microti. Because it does not sequester, Babesia microti can be seen in the blood with a microscope, whereas B. odocoilei cannot. The "experts" ignored the work of IGeneX laboratory in California. For most than a decade it 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. Babesia odocoilei infection is common. In 10,000 patient samples sent to them, they have found evidence of Babesia infection in 37.5%, vs. just 31% for Lyme disease. 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). Recently NC State's IPRL invented a PCR test for B. ocodoilei and published their finding of this parasite in 7 persons who are chronically ill. Dr. Lindner has found that this infection is common in his patients with fatigue, brain fog, and other medially-unexplained symptoms. It causes various symptoms and disabilities that range from minimal to severe. It is the cause of much, if not most chronic fatigue and "chronic Lyme disease" in the population of North America. Dr. Lindner and other ILADS-associated physicians are working to find additional proof of this infection and its fibrin-sequestering strategy. This infestation should soon be common knowledge in the mainstream medical community, but it depends upon how stubborn they will be.

Death from Hemophagocytic Syndrome:

His daughter's babesiosis-related symptoms and disability were gradually improving with time, but she still could not function sufficiently well to live on her own at grad school. In November of 2023, as a result of taking high lumbrokinase and nattokinase doses for 3 weeks--the longest stretch ever--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. To control her inflammation, she needed an incredible 3,000mgs of dexamethasone daily for 3 days (equivalent to 21,000mgs of prednisone). She developed severe fatigue, widespread pain, and worse abdominal pain and nausea. As usual, to try to lower the high corticosteroid need, she took several large tafenoquine doses. This worked to lower her corticosteroid need, but when it dropped precipitously, to almost nothing, 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 struggling to breath and chose to be intubated and sedated. She was essentially unconscious from then on, but when awake briefly, we asked her if she was comfortable and she nodded "yes". She needed high oxygen levels and pressures to maintain her blood oxygen levels. Her skin began breaking down in many places. Her kidneys stopped working and she required dialysis. 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 would only give her the low dexamethasone dose of 60mgs/day--as advised by some experts. That was a small fraction of the doses that she had needed previously according to her symptoms. (This is why hemophagocytic syndrome is so often fatal--the corticosteroid doses given to patients are far too low.) When her bone marrow began failing to produce red cells, white cells and platelets, the hematologist finally admitted that she had hemophagocytic syndrome. Kidney dialysis had to be stopped because her blood pressure was too low. 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, but none was found on autopsy. She was far too ill to undergo exploratory surgery anyway. She expired during the morning of Dec. 9, 2023 when her heart stopped due to severe lactic acidosis. Her hemophagocytic syndrome was so severe that it is unlikely that any treatment could have prevented her death, and she had repeatedly told Dr. Lindner that she wanted to die. She was weary of fighting this disease. An state-mandated autopsy was performed. Dr. Lindner obtained tissue and blood specimens to send to the IPRL at NC State for testing--hoping that in her death more proof can be found of this infection. 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

See much more information about her life, including her Bartonella-induced attachment disorder at:

http://henrylindner.net/Valerie/Valerie.html