HOW DR. LINDNER WAS FORCED TO DISCOVER CHRONIC BABESIOSIS CAUSED BY BABESIA ODOCOILEI (in construction)

For more explanation and for images of this disease and the effects of 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).

When his eldest daughter 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. Her cognitive dysfunction and intolerance of mental exertion worsened with time. By age 14 she was depressed and suicidal. Her mental stamina was helped by natural desiccated thyroid (NDT), but then worsened 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. A neurologist suspected multiple sclerosis. A brain MRI showed white matter hyperintensities--which are very rare in young adults.

Initial 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. Empiric antimicrobial therapy with doxycycline, then other antibiotics and antimalarials prescribed by a Lyme-literate medical doctor (LLMD) produced flu-like symptoms and mental distress and left her in a worse state. She especially could not tolerate antimalarial medications--they greatly worsened her mental pain--which she describes as an unbearable feeling of all negative emotions rolled up into one. Venous blood smears were negative for Babesia.

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 B. duncani. She had no B. microti antibodies. 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. Another neurologist diagnosed seronegative autoimmune encephalitis, but 5 days of high-dose intravenous methylprednisolone only worsened her condition. She could not take walks outside or watch videos with her family as such activities caused severe mental pain. By this time Dr. Lindner had consulted with many LLMDs, conventional Infectious Disease physicians, neurologists and psychiatrists. No one could help his daughter.

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). She had marked hemolysis accompanied by striking improvements in her mental and physical stamina, and decline in her prednisone requirement. She also had severe derealization and depersonalization. Her brain had clearly gone through a dramatic change.

During the subsequent months on AAAT, she had continual herxing and intermittent hemolysis, with only incremental improvements. (“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 immune-evading parasites are killed by anti-microbials and exposed to the immune system.) 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 at times.

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 deer ticks. 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, was proven 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 causing the red blood cells (RBCs) that they infect to become sticky--and thus to adhere to the linings of small blood vessels and to other RBCs. These species create nests in the small blood vessels. They reproduce and live out their lives there--avoiding the general blood circulation and the spleen. These nests block capillaries and post-capillary venules throughout the body and brain--causing dysfunction and inflammation in all tissues. This results in fatigue and a multi-organ dysfunction syndrome. Chronic babesiosis was previously described only in dogs infected with B. canis (Malherbe 1956, Sanders 1937). He realized that B. odocoilei must sequester in the capillaries and venules--which would 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 nests. One week later her urine again turned red-amber, and then green-black with higher hemoglobin and protein levels. She became more ill and required higher prednisone doses. Treatment was halted. Repeated cycles of lumbrokinase and AAAT had the same effects. 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.

In May of 2021, she tested positive with TLab’s recently developed B. odocoilei FISH test, indicating active infection with this Babesia species. After 21 months of antibabesial therapy, a repeat PET/MRI scan revealed greatly improved metabolism in her inferior frontal, temporal and parietal lobes. She now can 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 and emotional activity brought more blood flow to previously under-used parts of her brain, killing more Babesia and clearing more nests. She again required high prednisone doses to tolerate the resulting inflammation in her brain. Today the amount of heme and protein in her urine is much lower, when it does appear. Her blood counts and chemistries are normal. After 28 months of the most aggressive antibabesial regimen ever given to a human being, her brain is still infested with Babesia nests--and even though much improved she is still sick. This parasitic infestation is very hard to eradicate. (Most persons, fortunately, are not 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.)

Dr. Lindner is informing ILADS physicians and the mainstream medical community about this disease. He has contacted experts at the Pennsylvania Dept of Health, CDC, IDSA, and academic centers. He has submitted papers on B. odocoilei to several journals. Infectious Disease experts should have anticipated this disease because B. odocoilei is in ~20% of the deer ticks in Pennsylvania and in a similar percentage throughout the eastern US and Canada. Many persons are infected with this parasite. 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 have found evidence of Babesia infection in 37.5%, vs. just 31% for Lyme disease.

Soon after Dr. Lindner realized that the organism infecting his daughter was B. odocoilei, a tick expert published molecular proof of ongoing B. odocoilei infection in two persons with chronic babesiosis (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. This common infestation will soon be common knowledge in the mainstream medical community. Dr. Lindner and other ILADS-associated physicians are working to publish additional proofs of this infection and unique pathophysiology.