Archive for the ‘Bartonella’ Category

Head Trauma, Prolonged Neurological Symptoms, & Lyme Disease

Head trauma, prolonged neurological symptoms, and Lyme disease

By Daniel A. Kinderlehrer MD

When Brian finished college, he had dreams of becoming a professional hockey player. Unfortunately, he got a rough blow to the head and sustained a concussion. Although he didn’t lose consciousness, he developed a host of symptoms that led to leaving the ice.

He complained of daily headaches that were worse with exertion, physical and mental fatigue, decreased concentration and short-term memory, joint pains, muscle pains, muscle cramps, chest pain, sore soles that were more tender when first getting out of bed, paresthesias (pins and needles sensations) in his fingers and toes; daytime sweats and urethritis—pain on urination.

Sound familiar? Brian had spent time in upstate New York and went to college in Massachusetts. He had never seen a tick attachment nor an EM rash. An alert physician ran a Lyme Western Blot test but the only positive band was the IgG 18 kd, which was interpreted as negative.

The plot thickens

Because of his ongoing urethritis, Brian was put on Cipro for one week and all his symptoms flared. Later he was prescribed Levaquin, but he suffered the same reaction and stopped it after two days

Brian got checked out by specialists at a highly regarded medical center, but they could shed no light on the matter.

Brian’s symptoms were getting worse, including a sore throat with swollen glands. He had another Lyme Western Blot (performed at Labcorp) in which the IgM was now reactive at 23 kd. This was interpreted as positive for Lyme disease.

He was then prescribed doxycycline 100 mg twice daily. He herxed for five days and over the next two months he experienced mild improvement.

Post-Concussive Syndrome

I’m going to take a break from Brian to discuss post-concussive syndrome (PCS), symptoms that persist after a traumatic brain injury (TBI). The symptoms of PCS include headache, dizziness, neck pain, exercise intolerance, irritability, anxiety, sleep problems, diminished cognition with memory loss, poor concentration and difficulty with problem-solving, noise and light sensitivity.

In 2019, Sergio Azzolino and colleagues published a report entitled “The prevalence of Lyme disease and associated co-infections in people with a chronic post-concussive syndrome.”1 They wondered if patients with TBIs who continued to have symptoms of post-concussive syndrome a year after their head trauma had undiagnosed Lyme disease.

They did a retrospective chart review of patients who fit the criteria of ongoing symptoms of PCS at least a year after suffering a TBI. To be included in the study, patients had to have a negative brain computed tomography (CT) or magnetic resonance imaging (MRI) scan. Participants were excluded from the study if they had previously tested positive for Lyme and/or co-infections; had two weeks of antibiotics since the date of injury; had been diagnosed with a primary neurological illness (e.g., seizure disorder or multiple sclerosis), or had post-stroke syndrome.

The researchers tested 69 patients who met those criteria: 38% had a positive IgM Western Blot and 26% had a positive Western Blot IgG. They also tested 18 patients without a history of TBI but who had symptoms consistent with PCS: 72% had a positive IgM Western Blot and 33% had a positive IgG Western Blot.

IgM in Lyme disease is not only acute infection

The IgM antibody is considered an acute phase reactant—acute in medicine means recent onset. In most infections, the IgM antibody to a pathogen starts rising soon after the onset of infection. Then begins its decline about a month later, when IgG–the chronic phase reactant–starts increasing. Usually, the IgM becomes negative and the IgG remains elevated while the infection is still active, but IgG can remain elevated long after the infection has been eradicated.

However, this is not the case with Lyme disease. In Lyme, the IgM does indeed rise early—it is usually detectable within one to two weeks. But if the infection is untreated, the elevation in IgM will persist.2,3 This may be due to changes in outer surface proteins on the bacteria that continually signal a new infection to our immune systems.

In the series by Azzolino et al., IgM positivity was disproportionately higher than IgG.  And the same was true in the group of people who had the neurological symptoms of PCS without a history of TBI.

Most of my patients present with chronic persistent Lyme disease that has not been previously treated—they have been ill for years or even decades. The vast majority have Western Blot IgM positivity disproportionate to IgG positivity. It is not unusual for these patients to be told that the positive IgM is a false positive, since they have been ill for a long time and do not have an acute infection.

Prolonged neurological symptoms after TBI may be caused by Lyme disease

It turns out that a significant number of folks who get banged in the head and develop prolonged neurological symptoms were already suffering from a dormant infection with Borrelia burgdorferi, the Lyme pathogen. We know that some people get a tick attachment but don’t see a rash and don’t experience acute Lyme disease—but weeks, months or years later they become ill with chronic Lyme disease.

Sometimes, the symptoms develop gradually, but often they develop almost overnight. In the latter situation, there is usually a trigger—a viral infection, mold exposure, taking an agent that suppresses the immune system like corticosteroids, a vaccine, emotional stress, and trauma of any kind—especially head trauma.

Dr. Chad Prusmack is a neurosurgeon in Denver who sees a lot of patients with head trauma. He is unique among neurosurgeons in that he also diagnoses and treats Lyme disease. Chad told me that in his clinical experience, a third of his patients with PCS have Lyme disease and improve with appropriate treatment.

He also notes that most of these patients have issues with mold sensitivity and mold toxins, as well as dysautonomia, especially POTS—Postural Orthostatic Tachycardia Syndrome–and they improve considerably when they are stabilized.

Back to Brian

When I initially saw Brian, I told him I didn’t know how much his neurological symptoms were still attributable to the TBI he sustained over a year earlier as opposed to symptoms caused by the tick-borne diseases.

I suspect many readers of have already surmised that Brian was suffering from both Lyme disease and bartonellosis. Morning pain on the soles of the feet, urethritis, daytime sweats, and Herxheimer reactions to Cipro and Levaquin are big tip-offs.

The short story is that with treatment Brian experienced a 100% remission. He wisely decided not to pursue a professional career on the ice, but instead went to medical school. At the time of this writing, he is completing an orthopedic residency.

When Brian was a fourth-year medical student, I asked him what attending physicians on the wards had to say about Lyme disease. His reply: “They think it’s a joke, it’s not real.” This level of denial among mainstream physicians is, distressingly, still quite common.

I talked with Dr. Azzolino recently. He told me his clinical experience has been similar to that of Dr. Prusmack, who found that treating his long-term PCS patients for their tick-borne infections “…resulted in a dramatic improvement in function and reduction in disability” in this patient population.

The bottom line is that head trauma can activate dormant infections that manifest with chronic neurological symptoms that overlap with those of PCS. Anyone with head trauma with persistent PCS should get checked for Lyme disease.

Dr. Daniel Kinderlehrer is an internal medicine physician with a private practice in Denver, Colorado, devoted to treating patients with tick-borne illness. He is the author of  Recovery From Lyme Disease: The Integrative Medicine Guide to the Diagnosis and Treatment of Tick-Borne Illness.


  1. Azzolino S, Zaman R, Hankir A, Carrick FR. The prevalence of Lyme disease and associated co-infections in people with a chronic post-concussive syndrome. Psychiatr Danub. 2019 Sep;31(Suppl 3):299-307. PMID: 31488744.
  2. Craft JE, Fischer DK, Shimamoto GT, Steere AC. Antigens of Borrelia burgdorferi recognized during Lyme disease. Appearance of a new immunoglobulin M response and expansion of the immunoglobulin G response late in the illness. J Clin Invest. 1986;78(4):934–939.
  3. Steere AC, et al. Lyme arthritis: correlation of serum and cryoglobulin IgM with activity, and serum IgG with remission. Arthritis Rheum.1979;22(5):471-83

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Bartonella for Clinicians


Bartonella for Clinicians

Introducing IGeneX Bartonella ImmunoBlots
Jul 15, 2021

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A Tick Bite at Age 6, Followed by More Than 40 Years of Health Problems

A tick bite at age 6, followed by more than 40 years of health problems

Marta Edmisten gave the following as public comments at the August 26 meeting of the federal Tick-Borne Disease Working Group.

Good morning, my name is Marta Edmisten. I am here today to talk about the impact tick-borne disease has had on me.

I had my first known tick bite around age 6, in 1980. I found a bump behind my right earlobe. I vividly remember my mom dropping the wriggling tick into a medicine dosing cup full of rubbing alcohol, which immediately turned red.

That was two years before Borrelia burgdorferi was officially identified and even more years before testing was available.

I am now 47 and currently live with two strains of babesiosis, two strains of Bartonella, active Lyme disease, as well as tick-borne relapsing fever.

My testing is recent and not “borderline.” This is after over five years of treatment. I am here to tell everyone that the adage that tick-borne disease is hard to get and easy to get rid of is simply not true for so many of us.

Within a year of my first tick bite, I developed endocrine issues so worrisome that I was followed by the head of endocrinology at DC’s Children’s Hospital for fourteen months. No cause was ever discovered.

Problems in school

By age 8, I suddenly developed attention and reading issues after having flawless testing results in kindergarten. I also struggled with a sudden onset of allergies and asthma. My joints would swell out of nowhere and ache. I was screened for juvenile rheumatoid arthritis. The results were negative.

By middle school I suffered from anxiety, depression, depersonalization, suicidal ideation, insomnia, memory issues, and confusion.

I was officially diagnosed with ADHD and dyslexia after getting less that 400 on the SATs. My GPA at the time was stellar. I worked really hard.

I got my second known tick bite in Rhode Island while I was in college. I had a bull’s-eye rash all over my neck. I was told it was a spider bite and sent home.

I was diagnosed with  SMI—serious mental illness—soon thereafter. For over two decades, I saw preeminent psychiatrists in Boston and New York City. I took all the pills–nothing worked. I was hospitalized multiple times. I voluntarily underwent electroconvulsive therapy (ECT) treatments.

By the time I was 36, my arms and legs often twitched uncontrollably and soon fatigue and pain made running my successful business impossible. At 40, my vision was so poor I was unable to read, walking was impossible, and I became incontinent. Multiple autoimmune diseases were suspected. I was finally tested for Lyme disease and co-infections in 2016. I started treatment soon thereafter.

I am no longer on psychiatric medications, just things to help me sleep. Physically, I am better, but I’m still extremely disabled. Just last fall, I spent months not recognizing my home or remembering that my closest friend had passed away over a year earlier.

I look perfectly normal — as long as I am seated. I live with extreme mobility issues, drenching sweats, intermittent fevers, neuropathy, immune dysfunction, pain that often makes sleep impossible, and cognitive issues that make my dream of becoming a social worker out of reach at this time. There are so many people with my story.  Please believe us.  Please help us.

Marta Edmisten lives in Maryland.


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The Added Battle For Lyme Patients: Coinfections

The Added Battle for Lyme Patients: Co-infections

Holtorf Medical Group

Lyme disease is slowly gaining the recognition it deserves as a complex and serious illness that can cause severe health problems if not treated early and properly.

Learn more about Lyme disease and its symptoms here

However, it is important to note that oftentimes Lyme disease patients are not just fighting the Lyme bacteria, but also other co-infections. More specifically, part of the complication with Lyme disease is that, when bitten by a tick, people can be exposed to other pathogens that also carry illnesses. These are called co-infections. A survey of chronic Lyme-infected individuals found:

  • 50% had at least one co-infection
  • while almost 30% had at least two

So, if you have Lyme disease, there is a chance some of your symptoms may be due to a co-infection.

Below we outline two of the most common Lyme co-infections, their respective symptoms, and how to receive a proper diagnosis:


First reported in 1990, bartonellosis is caused by an infection of Bartonella bacteria. These harmful bacteria are capable of infecting a wide array of organisms.

Bartonella bacteria are most commonly spread by fleas, ticks, and lice. There are several different types of this bacteria. For instance, sand flies in South America carry one strain of Bartonella while human body lice, globally, carry another. Today, scientists have detected 29 different strains of this bacteria with approximately 15 that are capable of causing bartonellosis in humans.

Once Bartonella has infected the body, they primarily occupy the inside lining of blood vessels, specifically, red blood cells, macrophages, and endothelial cells. Until recently, it was believed that cases of bartonellosis tended to be mild, acute, and had little risk of contributing to further disruption. However, doctors have started finding that Bartonella may result in chronic infection.

Depending on the strain of Bartonella, symptoms may vary slightly. Bartonella henselae causes “cat scratch disease” and is associated with a bump or blister at the point of infection, swollen lymph nodes, fatigue, headaches, fever, and body aches.

Carrion’s disease (Bartonella bacilliformis) is linked to miliary lesions that ulcerate or bleed, fever, joint pain, and liver and spleen enlargement.

Bartonella quintana’s trench fever causes a fever, rash, bone pain (predominantly in the shins, neck, and back), enlarged lymph nodes, encephalitis, and eye infections.

As Bartonellosis commonly affects the skin, a streak-like rash is perhaps the most indicator of this infection. Other indicators of the condition include: tremors, neurological issues, blurred vision, numbness in the extremities, and psychiatric manifestations.

When Bartonella is attacking an immune system weakened by Lyme, it is possible to develop a more severe manifestation of bartonellosis. Bartonellosis can lead to endocarditis (heart infection) and bacillary angiomatosis (tumor-like masses caused by an infection in blood vessels).

Because bartonellosis can affect multiple bodily systems, it is often misdiagnosed or dismissed by standard practitioners. Proper diagnosis of Bartonella can be conducted through a variety of testing measures including Western Blot, IFAs (Indirect Immunofluorescent Assay), and others.


Babesia is a parasite similar to malaria. Both fall into the category of piroplasm, which are organisms that infect red blood cells. Infection of babesia is called babesiosis and is the most common Lyme co-infection as well as the most common piroplasm infection among humans.

The first Babesia species was discovered in 1888 by Hungarian pathologist, Victor Babes. Since then, over 100 distinct strains of Babesia have been identified, but only a few are considered human pathogens. In fact, babesiosis has long been recognized as a disease of cattle and other animals but the first human case was not documented until 1957. A young Croatian farmer was infected with Babesia and died shortly after of kidney failure. By the 1960s, babesiosis cases were documented in North America, and the bacteria is recognized as a serious and potentially harmful human pathogen.

The strain of Babesia that most often affects humans is Babesia microti. Like Lyme, babesia may be transferred via tick. However, it can also be transmitted from mother to unborn child through the transfusion of contaminated blood. This quality makes babesia an exceptionally sinister threat.

Symptoms of babesiosis share several similarities with Lyme. However, it may be distinguished with an initial high fever and chills. Progression of the infection brings with it symptoms including fatigue, headache, sweating, muscle aches, chest and hip pain, and shortness of breath, or air hunger. Fortunately, symptoms of babesiosis tend to be mild and non-life-threatening. However, the mildness of the symptoms also means that the condition is often overlooked until symptoms become more severe.

Because Babesia targets red blood cells, babesiosis is often linked to a condition called hemolytic anemia. Hemolytic anemia is characterized by red blood cells dying at a faster rate than the body can produce new ones. Symptoms include: confusion, dark-colored urine, rapid heart rate, heart murmur, dizziness, fatigue, pale skin, jaundice, and swelling of the spleen and liver.

Unfortunately, when babesia goes untreated, it can lead to more severe complications, especially for immunocompromised individuals.

Because symptoms of babesiosis are largely non-specific, especially early on, it is easily missed by standard practitioners. A blood test is required to check for signs of a Babesia infection. It is also important to check if there are other conditions present with babesiosis such as Lyme disease for optimal treatment.

Final Thought

Patients treated at Holtorf Medical Group have seen an average of 7.2 different physicians prior to their visit to our center, without experiencing significant improvement.

At Holtorf Medical Group, our physicians are trained to utilize cutting-edge testing and innovative treatments to uncover the root cause of your symptoms and treat the source. If you are experiencing symptoms of Lyme disease, a co-infection, or if you have been previously diagnosed, but aren’t getting the treatment you need, call us at 877-508-1177 to see how we can help you!


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Can Lyme Disease Trigger An Autoimmune Disease?


elderly man with Lyme disease and autoimmune disease taking his temperature

An increasing number of studies indicate that Lyme disease may ignite an autoimmune reaction in some individuals or symptoms may mimic an autoimmune disease. In their report, “Lyme arthritis presenting as adult-onset Still’s disease,” researchers describe the first known case of Lyme disease triggering Adult-Onset Still’s Disease, an auto-inflammatory condition that can impact the entire body (systemic disease).

Adult-onset Still’s disease (AOSD) is often thought to be an autoimmune disease, but is, in fact, a systemic auto-inflammatory condition, believed to be caused by an over-reactive immune response to an infection, such as Lyme disease. As Cimmino points out, both diseases share several clinical characteristics.¹

Still’s disease can cause “a triad of high fever, salmon-colored nodular rash and arthritis and/or arthralgia,” explains Ocon in the British Medical Journal.² Lyme disease can also present with fevers, atypical rashes and arthritis and/or arthralgias.

Both conditions were first identified in children. Still’s disease was initially considered a severe version of juvenile idiopathic arthritis (JIA), while Lyme disease symptoms were originally attributed to juvenile rheumatoid arthritis (JRA).

Lyme disease and autoimmune diseases

A growing number of studies indicate that Lyme disease may trigger an autoimmune response in some individuals or symptoms may mimic an autoimmune disease.

The authors suggest, “[Lyme disease] could be a great mimicker of other autoimmune diseases like DM.”

Case Presentation: Still’s disease

A 61-year-old man presented with a “complaint of intermittent spiking fevers, night sweats, generalised malaise, as well as a history of erythematous circular rashes on his right upper extremity,” writes Ocon.²

He was diagnosed clinically with Lyme disease and received two 10-day courses of doxycycline, but continued to suffer from fevers, chest pressure, a dry cough, along with malaise and arthralgia.

The man was subsequently diagnosed with Still’s disease, as he met the criteria with a fever greater than 102.2°F for at least 1 week; a characteristic rash; a white cell count of at least 10,000; lymphadenopathy, and elevated liver transaminases.

He was treated successfully with intravenous steroids and anakinra (a humanised interleukin-1 receptor antagonist), which is used to modulate the immune system.

Author’s Takeaway:

“For the first time, we describe a case of AOSD precipitated by Lyme disease.”

“Lyme disease is a rare trigger of adult-onset Still’s disease, likely mediated via immune system inflammatory activation.”

“AOSD presented with a rare manifestation of haemorrhagic pericarditis and tamponade.”

“We believe that the immunological response to Lyme disease may have triggered AOSD via a hyper-activated immune system.”

UPDATED: July 1, 2021

  1. Cimmino MA, Trevisan G. Lyme arthritis presenting as adult-onset Still’s disease. Clin Exp Rheumatol. 1989;7(3):305-308.
  2. Ocon AJ, Kwiatkowski AV, Peredo-Wende R, Blinkhorn R. Adult-onset Still’s disease with haemorrhagic pericarditis and tamponade preceded by acute Lyme disease. BMJ Case Rep. 2018;2018:bcr2018225517. Published 2018 Aug 16. doi:10.1136/bcr-2018-225517
  3. Cross A, Bouboulis D, Shimasaki C, Jones CR. Case Report: PANDAS and Persistent Lyme Disease With Neuropsychiatric Symptoms: Treatment, Resolution, and Recovery. Front Psychiatry. 2021 Feb 2;12:505941. doi: 10.3389/fpsyt.2021.505941. PMID: 33603684; PMCID: PMC7884317.

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